Wednesday, May 27, 2015

The "Insulation Theory of Junk DNA"

My copy of Junk DNA by Nessa Carey has arrived and I'm working my way through it. It really is as bad as we imagined.

Here's an example (pp. 34-36). She describes a situation where an angry baboon might smash an expensive watch. If you hide the watch in large rolls of insulation, the baboon is less likely to cause damage.
And the insulation theory of junk DNA was built on the same premise. The genes that code for proteins are incredibly important. They have been subjected to high levels of evolutionary pressure, so that in any given organism, the individual protein sequence is as good as it's likely to get. A mutation in DNA—a change in a base pair—that changes the protein sequence is unlikely to make a protein more effective. It's more likely that a mutation will interfere with a protein's function or activity in a way that has negative consequences.

The problem is that our genome is constantly bombarded by potentially damaging stimuli in our environment. We sometimes think of this as a modern phenomenon, especially when we consider radiation from disasters such as those at the Chernobyl or Fukushima nuclear plants. But in reality this has been an issue throughout human existence. From ultraviolet radiation in sunlight to carcinogens in food, or emission of radon gas from granite rocks, we have always been assailed by potential threats to our genomic integrity. Sometimes these don't matter that much. If ultraviolet radiation causes a mutation in a skin cell, and the mutation results in the death of that cell, it's not a big deal. We have lots of skin cells; they die and are replaced all the time, and the loss of one extra is not a problem.

But if the mutation causes a cell to survive better than its neighbours, that's a step towards the development of a potential cancer, and the consequences of that can be a very big deal indeed. For example, over 75,000 new cases of melanoma are diagnosed every year in the United States, and there are nearly 10,000 deaths per year from the condition. Excessive exposure to ultraviolet radiation is a major risk factor. In evolutionary terms, mutations would be even worse if they occurred in eggs or sperm, as they may be passed on to offspring.

If we think of our genome as constantly under assault, the insulation theory of junk DNA has definite attractions. If only one in 50 or our bases is important for protein sequence because the other 49 base pairs are simply junk, then there's only a one in 50 chance that a damaging stimulus that hits a DNA molecule will actually strike an important region.
There are two obvious difficulties with the insulation theory of junk DNA. The first is that Nessa Carey believes that a lot of noncoding DNA is functional. If she's correct, that requires a great deal of insulating DNA if it's going to protect the functional parts. You can't have it both ways.

The second problem is that it doesn't pass the Onion Test. (I don't think the Onion Test is mentioned in the book but I haven't finished it yet.)

I'm sure you can come up with other objections.

Here's how I like to think of this explanation using the field of bullets analogy popularized by David Raup in his book Extinction: Bad Genes or Bad Luck.

Imagine an automatic machine gun in a pillbox firing 10 rounds a second. It swivels from left to right spraying bullets at random across a field. The enemy has only one grenade and in order to silence the machine gun, some soldier has to run across the field avoiding the bullets until he gets within throwing distance of the pillbox.

Will the soldier's chances be increased if he lines up side-by-side with 99 other soldiers (no grenades) and they all charge together? No.

What if all 100 soldiers line up in single file with the man holding the grenade at the back? That will work.

So, the only way that the insulation theory works is if the extra DNA forms a tight shield around the important functional DNA and physically protects it from cosmic rays or UV light. But this DNA is already "shielded" by a plasma membrane, a nuclear membrane, and various histones; not to mention all the other protein molecules, carbohydrates, and water molecules inside the cell. It's difficult to see what advantage DNA molecules have in direct shielding.

None of these problems are discussed in the book.


238 comments :

  1. Mmm have you considered that when replication of the DNA occurs there are errors in the replications by the DNA polymerase? And there for having lots of non coding DNA would then diminish the probabilities of errors in the coding regions (introns also play a good role in this buffering efect). Im not saying that what Im stating is true, but it is a good posibility.

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    1. Most mutations, by far, are due to errors of DNA replication.

      Let's consider an error rate of one in ten billion. If 10% of the genome is functional then that means 320 million base pairs. That means that one mutation will be introduced into functional DNA every thirty replications (on average).

      That value holds true even if you add 2880 million bases of junk DNA (90% of the genome). The extra junk DNA acquires mutations at the same rate as the functional DNA but it doesn't change the mutation rate of the functional DNA one iota.

      That argument fails on simple logic.

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    2. That's of course correct. If the mutation rate per BP and generation is constant then there's no effect of genome size or of percentage junk. I'm aware of one somewhat more plausible idea of buffering, in that we find that TEs tend to generate a lot of copies early on and then the insertion gets slowed down by some RNAs. This process seems to generate a certain number of TE insertions per generation, rather than insertion at a particular rate and this might result in some buffering.
      The other buffering hypothesis I'm aware of is that by increasing the size of intergenic regions you also increase the likelihood of crossing over and thus get less linkage disequilibrium. That in turn would increase the effective population size, with fewer fixations of slightly detrimental alleles and more fixations of slightly beneficial ones.
      Neither of these scenarios is what Carey is discussing here and neither of them is likely to explain junk in toto.

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    3. This is the same explanation, but let's put it in more explicit terms:

      The mutation rate is measured (and physically occurs) per bp. So if you have a per-generation mutation rate of ~1x10^(-8), this means that each and every bp in the genome has a probability of 1x10^(-8) of acquiring a mutation (this is simplistic - in reality the mutation rate varies a bit along the length of the genome due to a number of factors, but we will ignore this here),

      So if the genome was 60Mb, and almost entirely coding sequence (there are such eukaryotes) it would acquire 6x10^7*10^(-8) = 0.6 mutations per generation in coding sequences. If the genome was 3Gbp with 60Mb of coding sequence, it would acquire 3x10^9*10^(-8) = 30 mutations per generation, of which (6x10^7/3x10^9)*30 = 0.60 mutations would be in coding sequence.

      One has more basis for advancing that argument with respect to transposable elements, but only if there was a constant number of TE insertions over the whole genome per generation (then they would be spread over a larger sequence space). However, this has serious population genetics problems, and it also fails in terms of the constant number of insertions premise - because the genome grows largely by TE element insertions and when you insert a new copy, that copy would be (not always, but often) an active non-degenerate copy, which would raise the potential number of insertions in the next generation. So the large amount of TEs in the genome does have a buffering effect but only because there are elaborate systems to generally keep TEs in check, i.e. that's not a selected effect but a side effect of what has come to be through largely neutral mechanisms, The system would be much better off if there were no TEs but it has no ways of getting there.

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    4. Note: I started typing this before Simon's post above

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    5. Hi Georgi

      I was wondering along those lines in an earlier inquiry to you:
      http://tinyurl.com/pewlze2

      Humor me:

      A species may not be able to get rid of its TEs, but a species may adapt to rein in its TEs.

      One such adaptation to "rein in" or suppress TE insertional mutagenesis could feasibly be "facultative heterochromatin" formation for those regions of genome whose genes' expression is temporarily not required.

      That means facultative heterochromatin (as just one for example) may subsequently represent an exaptation for higher level gene control that is “exuberantly” redundant.

      This can all occur even (neah - especially) if there was no positive selection at the organism/population level for the build up of the afore-mentioned bulk DNA.

      All we need do is invoke initial selection at the level of selfish DNA (for lack of a better term) or as Graur would call it "indifferent DNA".

      Forgive my persistence, what am I getting wrong?

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    6. On to the Onion test:

      Let's say this line of conjecture above has merit. The Onion Test still represents a problem.

      The c-value paradox is not puzzling when comparing onions to say metazoan lineages; but rather, very very puzzling when comparing some lineages of onions to other lineages of onions.

      This is why I attempted to rework on of Doolittle's metaphors
      http://tinyurl.com/kyfkw3j

      Allow me to rework one of Doolittle’s metaphors. My computer might be 10 ft from the wall socket, but it only has a 5 ft cord. I can solve the situation by using an extension cord (analogous to “spacer DNA”). Ideally, the extension cord need only be another 5 ft. Bringing in a 10 ft or even a 15 ft extension cord will also do the job.

      However, selective advantage in this case is not proportional to the added length of the cord. That is what I meant earlier by +/- multiples within certain parameters such that one lineage of onion may have more bulk DNA than another lineage of onion while doing the same job, as it were.

      I note that Graur (of Genetic Load fame) also seems to agree along these same lines:

      Graur: It has been pointed to us that junk DNA, garbage DNA, and functional DNA may not add up to 100% because some parts of the genome may be functional but not under constraint with respect to nucleotide composition. We tentatively call such genomic segments “indifferent DNA.” Indifferent DNA refers to DNA sites that are functional, but show no evidence of selection against point mutations. Deletion of these sites, however, is deleterious, and is subject to purifying selection. Examples of indifferent DNA are spacers and flanking elements whose presence is required but whose sequence is not important.

      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3622293/


      Negatively super-coiled topological domains & the P53 story jumps to my mind. Furthermore, sizes of those domains need not be "precise" to still be functional. As long as activated genes are found within a negatively-supercoiled region, the actual size of those domains may be very "imprecise" and explain the c-value paradox from one lineage of Onion to the next.

      Meanwhile, given this level of gene control was already admitted to be exuberantly redundant, c-value variation becomes moot, as it were.

      It cannot be that easy! I am surely missing something. I thank you in advance for your patience and your indulgence for any correction you provide.

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    7. For something to be an exaptation, it needs to be maintained by purifying selection, There is no evidence or theoretical reason to think this is the case with most of the human genome.

      There are extremely strong selective pressure to have effective (relatively speaking) mechanisms for silencing TEs. But that's a different subject.

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    8. Hi Georgi

      re

      For something to be an exaptation, it needs to be maintained by purifying selection

      Why can not that "something" be established first by selection at the "selfish or parasitic" gene level.

      No matter, I refer you to Graur:
      Indifferent DNA refers to DNA sites that are functional, but show no evidence of selection against point mutations. Deletion of these sites, however, is deleterious, and is subject to purifying selection.

      re
      There are extremely strong selective pressure to have effective (relatively speaking) mechanisms for silencing TEs. But that's a different subject.

      But but but...

      That was my whole point! Mechanisms for silencing the TEs were co-opted for an exuberantly redundant level of gene control.

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    9. Simon, The other buffering hypothesis I'm aware of is that by increasing the size of intergenic regions you also increase the likelihood of crossing over and thus get less linkage disequilibrium.

      If you 'wanted' to increase the likelihood of crossing over, wouldn't you just increase the frequency of crossover? There is no information about gene boundaries in meiosis. Crossovers tend to favour particular hotspots, and also regions of high sequence correspondence. The latter would actually tend to favour crossver within conserved regions (eg genes and their linkage neighbourhood) rather than between, in drifting sequence.

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    10. Me: There is no information about gene boundaries in meiosis.

      Though I did prompt myself to do a bit of digging, and it is clear that recombination does gain some information about genes, whether directly (through recognition of transription binding sites) or indirectly (by being selected against more inside ORFs than outside). http://www.sciencemag.org/content/310/5746/321.full

      Hotspots are preferentially located near, but not inside, genes. Which still does not favour the 'recombinational spacer' hypothesis.

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    11. @Allan: You want to increase the likelihood of crossing over between functional sequences. IIRC the likelihood of indels increases at the crossing over site, which isn't good in the seuqnece. If you have a constant rate of X-overs per BP and increase the distance between two genes by some number of filler bases, you increase the chance of X-overs between the two genes in proportion to the number of intergenic bases.
      While X-overs do not occur at a constant rathe throughout the genome, any additional junk increases the probability, because the probability of x-overs in the additional junk is non-negative and it is additive to the probabiltiy of an X-over without it. I don't think this explains all or even most of junk (and it has no effect on organismal fitness. If anything this seems like a candidate for species selection).

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    12. The problem is, the selective advantage of any given additional filler between any two genes is likely to be minute, and temporary, since it depends on heterozygosity across the linked locus. OTOH, if we have a mechanism to preferentially target crossover to hotspots (which appears to be the case), we have a much more generally applicable means to reap any assumed benefit from them, and there is no need for spacer - hotspots already tend to keep them outside the genes, and obviate any need to distort proportions still further by lengthening the amount of genome that is 'outside genes'. I'm a bit lukewarm on population-level explanations for crossover in general, though. I think it's a necessary evil with interesting side-effects.

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  2. Before I forget it: Thank you for the shout out to David Raup. When I was 13 I got the german translation of "the Nemesis Affair" for X-mas (I also have to give a shout out to whoever made the decision to give the book its German title "Der Untergang der Dinosaurier". It's of course somewhat misleading, but it mislead my parents into buying it for me) and it turned me from a kid fascinated with dinosaurs to a kid fascinated by statistical invertebrate paleontology. That fascination never left me and I'm very happy that I actually get to do this type of stuff. But I still get goosebumps every time I go to fossilworks, because that's of course the updated version of Sepkoskis handbook.

    As to the field of bullets analogy - that's based on a statistical technique developed by Hurlbert, Simberloff, van Belle and Heck, which Raup first applied to fossil data. And to come full circle, it's something that had some mathematical lose ends, which I recently got to tie up...

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    1. I took a grad course from Dave Raup. I forget the title, but it was about models in paleontology. Every couple weeks we had to build some kind of mathematical model or simulation to test some evolutionary or paleontological question. I recall particularly building a 3D morphospace of Darwin's finch beaks. Interesting and valuable course.

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    2. People often think that Stephen Jay Gould was the chief proponent of the Punctuated Equilibrium view. When I lecture on that topic in my Evolutionary Genetics undergraduate course, I put up a slide with photos of a more complete list of proponents: Steve Gould, Niles Eldredge, Jack Sepkoski, and Steven Stanley. But first in the list I put David Raup, who was perhaps the most influential of these. He really did marvelous quantitative studies (clade shapes, with Gould, for example).

      And this praise is coming from a non-punctuationist.

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    3. John,

      Did Dave Raup also teach you that Darwin finches with the small and large beak are different species?

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    4. @Larry: If I had expanded the list to just another person or two, hers would probably have been one of the names.

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    5. Inquirer,

      Why would this be relevant in a morphospace?

      Doesn't creationism require super fast speciation? Is there any evidence for the creationist claims that a dozen+ new species appeared per day after Noah's Flood-- and then slowed down enormously? If there's no speciation, isn't creationism just left speculating about unlimited miracles?

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    6. Diogenes,

      It all depends on how you define speciation.

      Does 2 base pair change out of 1.5 billion in the genome lead to the new species?

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    7. Inquirer, I'm responding just to tell you that there's a level of incoherence and ignorance that I won't respond to. You usually reach that level. As here.

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    8. For those interested:

      "Peter and Rosemary Grant are distinguished for their remarkable long-term studies demonstrating evolution in action in Galápagos finches. They have demonstrated how very rapid changes in body and beak size in response to changes in the food supply are driven by natural selection. They have also elucidated the mechanisms by which new species ariseand how genetic diversity is maintained in natural populations. The work of the Grants has had a seminal influence in the fields of population biology, evolution and ecology."

      Wikipedia

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    9. So, it looks like 2 base pair change out of 1.5 billion in the genome meets the criteria of a new species by some unknown definition. Evolution in action. Too bad this definition is so fluid it resembles the flood. Lol

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    10. Inquirer, what are you blathering about here? Does it have anything to do with the topic? Where do you get this "2 base pair change" from?

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    11. 2 bp - probably not, but it would depend on the exact consequences of those 2bp changes. There is no mutation rate per speciation event.

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    12. It is possible to get complete post-zygotic reproductive isolation from only two fixations. But unlikely. Suppose two geographically isolated populations of one species, with two loci, with all genotypes in both populations aa, bb. New allele A, compatible with both a and b, becomes fixed in one population, and new allele B, compatible with both a and b, becomes fixed in the other, let's say by drift. Now the two populations have different fixed genotypes; AAbb and aaBB. Sadly, A and B are incompatible and if both are present, as they would be in any hybrids between populations, the result is lethality in the early embryo. Viola, two species.

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    13. @John: I seriously envy you. I think my post shows that there's a fair bit of hero worship on my part regarding Raup and I only know him from his writings.
      @Joe: Which of the MBL papers were you referencing there (they are all great and all of them have Raup and Gould as authors, though not all of them as the only ones).

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    14. @ John Harshman,

      "It is possible to get complete post-zygotic reproductive isolation from only two fixations. But unlikely. Suppose two geographically isolated populations of one species, with two loci, with all genotypes in both populations aa, bb. New allele A, compatible with both a and b, becomes fixed in one population, and new allele B, compatible with both a and b, becomes fixed in the other, let's say by drift. Now the two populations have different fixed genotypes; AAbb and aaBB. Sadly, A and B are incompatible and if both are present, as they would be in any hybrids between populations, the result is lethality in the early embryo. Viola, two species."

      Can you apply the same formula to humans?

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    15. Can you apply the same formula to humans?

      Of course you can. Why not? Of course it would require that two geographically isolated populations of humans exist long enough for two such alleles to arise and become fixed. And it requires that the alleles with the stated properties must exist, which seems rather rare. Then again, something fairly similar seems to happen reasonably often in plants, where it occurs because of frequent gene duplication and loss.

      Why do you ask?

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  3. "Most mutations, by far, are due to errors of DNA replication."

    That's the key point (it should be in the opening post!).

    However, there clearly is some kind of relationship between radiation damage and mutation. Some questions I am curious about (anyone have answers?):

    1. Is background environmental radiation really the cause of any substantial proportion of mutations in the wild? Or is it only in artificial settings, where we bombard experimental organisms like fruit flies with ridiculous amounts of radiation, to induce mutations?

    2. In experimental mutagenesis, cancers caused by mutagens, etc., are the mutations mostly caused by

    (a) direct radiation damage to DNA, or

    (b) more generic damage to cells (e.g. free radicals causing chain-reaction ionization, straight-up physical damage, etc.), which causes healing responses etc., which increases replication rate, which increases mutations because there are more replications.

    Option (b) would explain how various kinds of non-radiation mutagens work (e.g. asbestos).

    Cheers! Nick

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    1. Nick,

      What is the other cause of mutations other than replication errors and radiation?

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    2. Nick - Don't really know, but 'natural' free radicals are a significant source of mutation, particularly in mitochondria where they are produced in abundance as part of their activity. They have minimal genomes and hence somewhat reduced replicase errors per genome-copy compared with nuclear genes. I'd say that, in them, the balance may shift appreciably away from replication as the principal mutational source.

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    3. Pet peeve alert

      People often claim free radicals as the main thing in mitochondrial mutation, but the support for this is quite poor. This is most well studied in vertebrate mitochondria, so insert the caveats, but at least Drosophila work backs it up. A major product of oxidative damage is and 8-oxo-dG adduct, (bad phenol during DNA extraction will do plenty of this for you) which is supposed to paired to A, leading to G-T transversion. But in vitro data suggests that the mitochondrial polymerase actually does not make this mistake very often across from an 8-oxo-dG, but most often stalls replication at the site. And, the mutational profile in mitochondria is strand specific, and transition heavy. These are hard to consolidate with a random oxidative-damage model of mutagenesis.

      Two papers (that I was not a part of) pressing this point;

      http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1003794

      http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1003974

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    4. Fair enough, though DNA damage would seem a prime candidate for an adaptive superoxide mop-up mechanism. Is there a normal mutation rate in cells deficient in one or another mechanism, do you know?

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    5. We are working with some tissue from a SOD2 knockout now. I'll get back to you.

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  4. If I can piggyback on your question no. 1: Does anybody here know where the claim that cosmic rays are the main source of mutation comes from? I've lost count of the number of times I've seen physicists make this claim either in print or on video.

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    1. DAK: Does anybody here know where the claim that cosmic rays are the main source of mutation comes from?

      I've never seen any physicist make this claim. I've seen creationists pretending to be scientists make this claim hundreds of times.

      It's bullshit. Replication errors almost always dominate hits from radiation.

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    2. I've come across this numerous times - especially astronomers.

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    3. One of the earliest references I've found was Carl Sagan's The Cosmic Connection where he speculates that human evolution was driven by a nearby neutron star. I assumed that this is where most of these physicists are getting the idea from since it fits the age group and time of publication. I don't know if Sagan is the original source of this or not though.

      As I said, it's very common. I found some lecture notes for a Astro course at Stony Brook where this very claim is laid out as the main source of DNA mutation.

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    4. DAK: I've come across this numerous times - especially astronomers.

      Astronomers are not physicists. Unless they're astrophysicists.

      I found a link once, I believe from NASA, saying that most mutations are not caused by cosmic rays (obviously few of those reach the surface) but I can't re-find the link now despite googling. Background radiation, I don't know about.

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    5. In "Cosmos" Carl Sagan mentions cosmic rays as an example that life is exposed to mutagens. Not as the main source for mutations. He probably didn't know back then about what, if any, would be the main source of mutations, so his example was one of several possibilities.

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    6. You know that science advances, right?

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  5. The mistake Nessa Carey has made was also made some years ago by an ecologist, who noted that the rate of clearance (by floating logs and violent waves) of intertidal seashore life would be greater in large patches of those organisms.

    I was listening to some ecologists discuss this, and said "wait a second, is this like saying that your chance of being hit by a meteor is greater if you live in a large country?" This seemed to cast a sudden pall over the discussion.

    Actually, Carey has made the opposite mistake, thinking that your chance of being hit by a meteor is smaller if you live in a large country.

    It's something about numerators and denominators, and some biologists and some science reporters aren't too good with those.

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    1. Joe Felsenstein; Wednesday, May 27, 2015 9:19:00 PM

      "The mistake Nessa Carey has made was also made some years ago by an ecologist, who noted that the rate of clearance (by floating logs and violent waves) of intertidal seashore life would be greater in large patches of those organisms."

      Carey's rationale is obviously flawed; however, you might what to read my paper in which I describe the protective role of the so called "junk DNA" against deleterious insertional mutagenesis by endogenous and exogenous inserting elements, particularly against insertional oncogenic transformation:

      http://biorxiv.org/content/early/2013/11/18/000588

      "In humans, for example, given the enormous number of somatic cells and their high turnover rate during reproductive span, without protective mechanisms, the number of insertion events, especially those associated with exogenous viruses such as retroviruses, that could lead to cancer would be evolutionarily drowning. A dramatic example of the problems associated with insertional oncogenic transformation is from the highly promising biomedical field of gene therapy using viral vectors, which has been devastated by high prevalence of cancer in treated patients [8-12]. It is relevant to mention also that insertional transformation has been one of the main and most effective approaches for identifying and mapping genes and regulatory elements implicated in cancer [13-15], which points to the tremendous selection pressure imposed by cancer-inducing insertion mutagenesis in multicellular 3 organisms."

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    2. Perhaps the quote above makes more sense in the context of the following excerpt from the same paper:

      "Key to exploring the hosts’ evolutionary constraints on the location and the amount of genomic jDNA, as well as it’s putative protective function, is the evolution of defense mechanisms in form of preferred or specific genomic sites for the integration of inserting elements in microbial organisms such as Bacteria, which have little jDNA. The evolution of these protective mechanisms is strong evidence for the selective pressure against insertional mutagenesis in these single-cell organisms. This selection pressure, however, take a new dimension in multicellular organisms, in which insertional mutagenesis occurs not only in the germline, but also in the somatic cells. Although the number of somatic insertional mutations during the course of the reproductive life span of multicellular organisms is enormous, because of the high turnover of cells in many tissues, most insertional mutations, including those causing cellular death, have a limited negative impact on the organism. The major problem is with the insertional mutagenesis that causes uncontrolled proliferation of cells, which can lead to neoplastic transformations, or cancer.

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    3. We've all been over your theory a million times, and I'm not going to do so again. Yes, the effect you claim is probably real. That puts you way ahead of Carey.

      If Carey's effect were real, then we could ask whether a small addition of junk DNA would have enough of an advantage to be effectively selected for. That is where your theory runs into trouble.

      But in her case the effect isn't even real, so we don''t need to ask the second question.

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    4. Joe Felsenstein; Thursday, May 28, 2015 6:35:00 AM:

      “We've all been over your theory a million times, and I'm not going to do so again. Yes, the effect you claim is probably real. That puts you way ahead of Carey.”

      That is true, you have address my theory a few times, but the question is: did you fully understand it?

      For example, have you understood the “somatic dimension” of my theory as it relates to cancer-inducing insertion mutagenesis in multicellular organisms, such as humans?

      Have you thought about the enormous number of insertional events by endogenous and exogenous inserting elements (such as retroviruses) at the somatic versus germline level?

      Please, let me give you some numbers that you might consider relevant in evaluating the putative selective pressure against insertional mutagenesis at the somatic level in humans.

      According to the latest estimates a human adult contains approximatively 3.72 × 10(13) cells ( http://www.ncbi.nlm.nih.gov/pubmed/23829164).
      Do you realize how many cells a human produces during the ontogenetic development up to the end of its reproductive period and how many somatic insertional mutations occur during this period?

      Do you realize that in a HIV infected individual there are approximately 10 (11) virions produced every day, (lhttp://www.ncbi.nlm.nih.gov/pubmed/23284080), leading to approximate 10 (9) newly infected host cells, that is 10 (9) new genome insertions per day?

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    5. Joe Felsenstein; Thursday, May 28, 2015 6:35:00 AM:

      “….we could ask whether a small addition of junk DNA would have enough of an advantage to be effectively selected for. That is where your theory runs into trouble.”

      With all due respect Joe, but this is a major flaw in understanding how selection, or for that matter neutral evolution, works in this particular case. Indeed, I don’t think that you have carefully read (if you did) my paper ( http://biorxiv.org/content/early/2013/11/18/000588), as I don’t think you’ll still be presenting this argument; please read my paper and let me know if you maintain it.

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  6. The theory predicts that at least some of the "junk" is structure or circuitry needed for proper (chemical) addressing of the gene action data.

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    1. That there's regulatory sequences was predicted and then found a very long time ago by actual scientists. Describing those features in a technology-isn way just shows, again, that you're a kook desperately looking for admiration. All you accomplish is to further demonstrate that you're an ignorant and an idiot.

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    2. That's nice. Let me know when you're done pontificating.

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    3. circuitry needed for proper (chemical) addressing of the gene action data.

      ... how to work toward getting a molecular biology manuscript rejected in one easy step. Hhaha

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    4. "That's nice. Let me know when you're done pontificating."

      Ironically says the professional pontificator.

      Sure Gary, we are all in awe at your Amazing Theory. See? Capitalized and bolded. That's so much admiration. You idiot.

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  7. So, asking as a layperson, is the following statement generally correct or incorrect/too simplistic:

    While mutational load is a good argument for a high percentage of junk, it's not a reason to draw the conclusion, as Carey apparently does, that the junk is there for the purpose of protecting against mutational load.

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    1. Fair enough: the more DNA you've got, junk or non junk, the more mutations and other kinds of damage you've got. So the functional fraction is not protected.

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    2. Speaking as a biologist who's specialty isn't genetics at this level, I'd say that statement is correct but unclearly expressed.

      We have lots of mutations (mutational load). Therefore, we end up with a lot of DNA that doesn't function usefully (junk DNA). However, it does not follow that junk DNA protects against harmful effects of mutations. The number of mutations is approximately proportional to the amount of DNA, so more DNA = more mutations. The number of mutations in useful DNA is proportional to the amount of useful DNA, and having much or little useless DNA doesn't change that. Therefore, junk DNA cannot have the function of preventing harmful mutations.

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    3. Regarding the junk DNA discussion: If all of our DNA were necessary, mutational load would ensure we'd have long since gone extinct. This does *not* prove that the reason we haven't gone extinct is because junk DNA "protects" the non-junk from mutation.

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    4. Hi Barb,

      I feel like I woke up in the middle of the movie “Ground Hog Day”!

      I am going to try this one last time by responding to your post which seems to align with what I was attempting above.

      I will recite Graur:

      Graur: It has been pointed to us that junk DNA, garbage DNA, and functional DNA may not add up to 100% because some parts of the genome may be functional but not under constraint with respect to nucleotide composition. We tentatively call such genomic segments “indifferent DNA.” Indifferent DNA refers to DNA sites that are functional, but show no evidence of selection against point mutations. Deletion of these sites, however, is deleterious, and is subject to purifying selection. Examples of indifferent DNA are spacers and flanking elements whose presence is required but whose sequence is not important.

      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3622293/

      Could somebody/anybody please explain to me how Graur’s observations are not relevant to this discussion?

      To my reading, Graur has clearly indicated that non-informational DNA can simultaneously

      1 – “show no evidence of selection against point mutations.”
      2 – ... “Deletion of these sites, however, is deleterious, and is subject to purifying selection.”

      I realize that this is NOT how ENCODE originally phrased their thesis.

      That said, my reading of Graur is in fact offering a cogent explanation of what would be deemed the non-junk status of DNA “spacers” and “flanking elements”

      If I am wrong – please show me where I err. If I am not wrong, would somebody please indicate I am not barking up the wrong tree?

      If in fact, these scribbles have any modicum of validity, the Onion Test has been passed and the mutational load rebuttal is moot, as explained above.

      Delete
    5. Could somebody/anybody please explain to me how Graur’s observations are not relevant to this discussion?

      Allowing for the possibility of something is not at all the same as claiming that it accounts for most of the genome

      Delete
    6. Hi Georgia

      So we are not debating "whether if" but rather "how much"?

      Have I got that right?

      Delete
    7. Could somebody/anybody please explain to me how Graur’s observations are not relevant to this discussion?

      In Graur's scenario, irrelevant DNA's sequence is not conserved but its length is. In your scenario, its length isn't conserved either. That's why Graur isn't relevant.

      Delete
    8. Damn auto-correct on iPhone

      I meant Georgi

      My apologies

      Delete
    9. Tom Mueller asks,

      Could somebody/anybody please explain to me how Graur’s observations are not relevant to this discussion?

      They are not relevant because Dan Graur is creating an unnecessary category of genomic DNA. There are only two categories of DNA; functional and non-functional. The non-functional component is called junk DNA.

      Functional DNA may be conserved because the sequence is important or it may be non-conserved because the sequence isn't important.We know for a fact that there is some non-conserved DNA that carries out an important function—mostly spacer DNA. It makes up only a small percentage of the genome.

      There are several bulk DNA hypotheses. If true, they would attribute a large percentage of genomic DNA to the category of functional DNA that is not conserved. Dan Graur calls this "indifferent DNA" but that terminology is unlikely to catch on.

      Delete
    10. Laurence A. Moran; Thursday, May 28, 2015 2:17:00 PM:

      "There are only two categories of DNA; functional and non-functional."

      Amen to that! The genomic DNA is ether functional or non-functional.

      Unfortunately, there has been a lot of confusion about that, some introduced by our most esteemed scientists:

      In one of the first papers addressing the notion of jDNA (6), David Comings writes: “These considerations suggest that up to 20% of the genome is actively used and the remaining 80+% is junk. But *being junk doesn’t mean it is entirely useless*. Common sense suggests that anything that is completely useless would be discarded.”

      In their iconic paper “Selfish DNA: the ultimate parasite” (7), Leslie Orgel and Francis Crick, summarize their thoughts as follows: “The DNA of higher organisms usually falls into two classes, one specific and the other comparatively nonspecific. It seems plausible that most of the latter originated by the spreading of *sequences which had little or no effect on the phenotype*.”

      More recently, in a publication addressing the ENCODE project (8), Sean Eddy, remarked: “These data support a view that eukaryotic genomes contain *a substantial fraction of DNA that serves little useful purpose for the organism*, much of which has originated from the replication of transposable (selfish) elements.”

      Although seemingly innocent, these citations are relevant examples of confusing statements about the functionality of genomic DNA. Some of this confusion might dissipate by recognizing that: (i) if genomic sequences *are not entirely useless*, (ii) if they *have little effect on the phenotype*, or (iii) if they *serve little useful purpose for the organism*, then, these DNA sequences are functional.

      Delete
    11. Is this the same Graur who embarrassed himself with the paper on genetic load argument and then retracted it when pointed it out to him he needed serious help with his math? Even PZ Myers fell for it.

      scienceblogs.com/pharyngula/2015/01/06/the-genetic-load-problem/

      Delete
    12. Hi Tom,

      Dan Graur's observations are relevant as he brings forward the fact that the genomic DNA can have non-informational functions. The obvious question is how much genomic DNA has non-informational functions and what are these functions.

      I think you are familiar with the nucleoskeletal and nucleotypic hypotheses, which have been promoted by Cavalier-Smith and Ryan Gregory, respectively, in dozens of scientific publications. You also know that Ford Doolittle embraces the nucleo-skeletal and nucleotypic theories as pillars of his theoretical framework on genome size evolution and genome functionality.

      What do you think about these hypotheses: are they correct or not?

      Delete
    13. "Common sense suggests that anything that is completely useless would be discarded."

      Many people thought this early on in junk DNA history. However, this "common sense" statement is laden with assumptions. For example, it requires that junk DNA can be removed from the genome as quickly as it accumulates. It was only after actual empirical data were gathered that scientists generally came around to the conclusion that a lot of our genome is junk. This is quite at odds with the ID creationist version of the story where the evil Darwinists assumed from the beginning that our genome is littered with junk as a personal insult to the Creator.

      I don't see why ID creationists are so interested in junk DNA anyway. If our genome was 100% functional or 99% junk, this would say nothing about the validity of evolutionary theory. It would also say nothing about the existence of a creator.

      Delete
    14. I don't see why ID creationists are so interested in junk DNA anyway. If our genome was 100% functional or 99% junk, this would say nothing about the validity of evolutionary theory. It would also say nothing about the existence of a creator.

      It says nothing about the existence of a creator who chose to create species using evolution (though such a creator would be redundant by definition). It does say something about the existence of a creator who takes a design role if you first require an entity with all the necessary knowledge and abilities, then have to specify that said entity was so careless or incompetent with the supposed pinnacle of creation that less than 10% of the genome works.

      Delete
    15. Inquirer is a sock puppet for Pest, as I'll show below. It is possible those two are sock puppets for someone else, perhaps Joe "Security Clearance" Gallien?

      Inquirer, above, writes: Is this the same Graur who embarrassed himself with the paper on genetic load argument and then retracted it when pointed it out to him he needed serious help with his math? Even PZ Myers fell for it.

      This should sound familiar, because sock puppets have written almost the identical ad hominem each time the topic of genetic load, or name "Graur" come up.

      On March 14, 2015, Pest wrote: "How about genetic load? Can anybody remember Dan Graur and his famous proclamation about how everyone of us including Larry & Joe F should have 7 x '10^45 children if ENCODE is right.

      Joe is an expert in PG so maybe he should speak first.
      Can anyone still stand by this proclamation?

      http://sandwalk.blogspot.ca/2015/01/a-lesson-on-genetic-load.html

      ...Oh, BTW: Dan [Graur] has kindly removed his post. It was a total embarrassment.

      I don't think he is going to admit he was wrong..


      And on March 15, Pest wrote: One of Larry's and the gang other favorites is the genetic load argument.

      Are you familiar with that?

      ...Also by Dan Graur:

      If @ENCODE_NIH is right, each of us should have 7 x 1045 children.

      It looks like Graur has removed the post ever since some have pointed it out to him that his calculations were way off.


      Let's compare more closely.

      Pest: Graur has removed the post ever since some have pointed it out to him that his calculations were way off.

      Inquirer: and then retracted it when pointed it out to him he needed serious help with his math?

      Note that the second clause is incoherent because the subject, which Pest gave as "some", has been deleted. Quite probably, the original version had a person (Joe Gallien??) claiming that "I pointed it out to him" or "ID proponents pointed it out to him" and later Inquirer copied and pasted this passage, but deleted the subject "I", leaving a gap.

      Pest: Oh, BTW: Dan [Graur] has kindly removed his post. It was a total embarrassment.

      Inquirer: Is this the same Graur who embarrassed himself

      So Pest is Inquirer, but what is relevant scientifically is that Pest/Inquirer knows that the genetic load argument, and Dan Graur, are serious threats to IDiocy, because anybody can understand the genetic load argument, and Graur treats the IDiots with the level of respect they deserve.

      So every time the topic of genetic load is raised, Pest/Inquirer immediately launches an ad hominem attack on Dan Graur, believing that that will smear the genetic load argument and somehow invalidate it. That's all he's got.

      We may also speculate if Inquirer is some third party, possibly Joe Gallien. Joe Security Clearance always pretends to be a scientist, not religious, so he could be using Inquirer as an outlet for his religious concerns.

      Delete
    16. judmarc says: " It does say something about the existence of a creator who takes a design role if you first require an entity with all the necessary knowledge and abilities, then have to specify that said entity was so careless or incompetent with the supposed pinnacle of creation that less than 10% of the genome works."

      Yes, I'll agree junk DNA may something about the nature of a creator, but it sheds no light on whether or not a creator exists. If ID creationism wants to make the argument that no junk DNA is evidence for a creator, they must make assumptions about this creator, for which they have no evidence. For example, that junk DNA is somehow aesthetically unpleasing to the creator such that (s)he/it would not allow junk DNA. How could anyone know that? Maybe the creator doesn't care if junk DNA accumulates in genomes. Or, as Diogenes has posited, maybe the creator made us to be vectors of broken transposons and repetitive DNA elements, his favored creations (and beetles, he's gotta love beetles, right?)

      Delete
    17. "Dingaling

      Did it........................................................shit get attracted to shit?"

      Translation:
      I'm very frustrated that my canned creationist BS gets rationally destroyed in every venue. Time to resort to lots of profanity and the lame 'origins' god of the gaps canard.

      Delete
    18. Dingaling

      That is too funny. When I pointed out a few months ago that Pest was really Quest, the fact that both had a habit of mocking a person's name was part of the evidence. Inquirer apparently forgot that, even as he is now denying that he is pest/quest.

      Delete
    19. ... or maybe it was that Johnny was really Quest, can't keep them straight anymore. Amazing how frequently truth and honesty is abandoned by god fearin' creationists.

      Delete
    20. If Pest is Quest, and since Inquirer is definitely Pest, then Inquirer would be Quest. Quest was Johnny and some other sock puppets.

      And Quest, of course, once let drop that he knew John Witton was in jail; when asked, many many times, how he knew this about Witton, Quest refused to answer, thus raising the possibility that Quest was Witton.

      Somebody's got a lot of time on his hands.

      Delete
    21. World's Greatest Quote Miner Diogenes,

      Inq. Wrote that Graur published a paper on genetic load and then retracted it. I never wrote that because I didn't know graur ever retracted a paper on genetic load.
      To prove your point that we are the same people cough up my quote on that or burn in hell.

      Delete
    22. Inquirer,

      Did you or did you not, as Pest, say that Graur removed his post on genetic load? I "coughed up" the quote proving that above. Did you or did you not write that Graur removed his post on genetic load? Please copy and paste the quote from you that I copied above. Copy and paste your own words. I copied them above. Why don't you copy your own words? Then try lying about them.

      Delete
    23. What the World's Greatest Quote Miner and Liar Diogenes does when caught in the act of lying and quote mining and not being able to provide evidence for his claims?

      He does what he does best when he can't cough up evidence; as if nothing happened he attacks straw man. What a shameless goof!

      Again, provide a link and a quote where " I said that Graur published and then retracted a paper on genetic load"

      If you don't, I will ignore all you comments and remind you regularly about this act of lying and quote mining.

      I know you won't, because I never said that, so burn in hell you lying, shameless piece of meat!

      Delete
    24. Pest, rather than admit he deceptively used Inquirer as a sock puppet, now bizarrely demands:


      Again, provide a link and a quote where " I said that Graur published and then retracted a paper on genetic load"


      Why should I provide a quote to back up something I never claimed? I never claimed you said Graur retracted a paper. You are lying when you accuse me of saying you said Graur retracted a paper. In fact, I said you said Graur removed a paper.

      If you don't, I will ignore all you comments and remind you regularly about this act of lying and quote mining.

      You cannot do both, idiot. You cannot both ignore my comments and also accuse me of lying.

      But go ahead and try. If you accuse me of lying, I will 1. Repeatedly post quotes by you where you indubitably lied, to start with, your last comment, 2. Since you're Quest, Larry will delete your comments since you're banned, and 3. My evidence will remain but your false accusations will be deleted.

      Delete
    25. Again, Inquirer/ Pest, you were lying when you accused me of saying you said Graur retracted a paper. I asked you a simple question: did you, or did you not, say that Graur removed a post? Simple question. You refused to answer this simple question because answering "yes" or "no" would reveal your dishonesty. Instead of answering this simple question, you just lied and accused me of saying you said Graur retracted a paper. You cannot answer simple questions and cannot back up your dishonest claims.

      Here is why you dare not answer the simple question I asked:

      On March 14, 2015, Pest wrote: How about genetic load? Can anybody remember Dan Graur and his famous proclamation about how everyone of us including Larry & Joe F should have 7 x '10^45 children if ENCODE is right.

      Joe is an expert in PG so maybe he should speak first.
      Can anyone still stand by this proclamation?

      http://sandwalk.blogspot.ca/2015/01/a-lesson-on-genetic-load.html

      ...Oh, BTW: Dan [Graur] has kindly removed his post. It was a total embarrassment.

      I don't think he is going to admit he was wrong..


      And on March 15, Pest wrote: One of Larry's and the gang other favorites is the genetic load argument.

      Are you familiar with that?

      ...Also by Dan Graur:

      If @ENCODE_NIH is right, each of us should have 7 x 1045 children.

      It looks like Graur has removed the post ever since some have pointed it out to him that his calculations were way off.


      The Genetic Load argument is such powerful evidence for Junk DNA and against Intelligent Design, the ID proponents all know that and they're all wetting their pants in fear. So they decided on a strategy of ad hominem attacks, lying and smearing, trying to attack the messenger rather than simply answer: how can every baby born have ~130 new mutations if all DNA is functional and all mutations are "catastrophic" as IDcreationists claim? No you can't answer that, so you try a strategy of lying and smearing Dan Graur and myself, believing that, via your lies and ad hominems, you can delegitimize the question and evade answering it.

      I will ask you again: did you or did you not, as Pest, say that Graur removed his post? A simple question a liar cannot answer. Intelligent Design proponents are such insane liars, you can't answer the simplest goddamn questions.

      Delete
    26. Then again, just because smart people are sometimes wrong doesn't mean that stupid people are right.

      Delete
    27. Hi Larry

      Re:
      LM There are several bulk DNA hypotheses. If true, they would attribute a large percentage of genomic DNA to the category of functional DNA that is not conserved. Dan Graur calls this "indifferent DNA" but that terminology is unlikely to catch on.

      I think it fair to call Graur’s "indifferent DNA" “functional albeit non-informational DNA. I hope I got that right

      Re:
      LM Functional DNA may be conserved because the sequence is important or it may be non-conserved because the sequence isn't important.We know for a fact that there is some non-conserved DNA that carries out an important function—mostly spacer DNA. It makes up only a small percentage of the genome.

      I think part of the problem is that I employed the term “spacer DNA” in a more generic fashion than precisely employed by most present. ITMT, Graur’s citation of “spacers and flanking elements” were cited as examples only and were neither comprehensive nor exhaustive a list of “indifferent DNA”.

      In an earlier post I wondered out loud a regarding Peter Fraser’s extraordinary results:

      Somehow, all that intervening non-informational DNA is alternately and differentially exposing/sequestering crucial bits of expressed/nonexpressed DNA according to the developmental/differential/environmental response status of the cell.

      Georgi came up with a patient and indulgent response that still missed the original thrust of my line of inquiry IMHO

      http://sandwalk.blogspot.ca/2015/05/ford-doolittle-talks-about-transposons.html?showComment=1431447899713#c2828632287249353847

      I think the problem is my age and penchant for using old fashioned terminology that has fallen out of common usage. I direct our attention to

      Facultative heterochromatin

      The regions of DNA packaged in facultative heterochromatin will not be consistent between the cell types within a species, and thus a sequence in one cell that is packaged in facultative heterochromatin (and the genes within are poorly expressed) may be packaged in euchromatin in another cell (and the genes within are no longer silenced). However, the formation of facultative heterochromatin is regulated, and is often associated with morphogenesis or differentiation. An example of facultative heterochromatin is X-chromosome inactivation in female mammals: one X chromosome is packaged as facultative heterochromatin and silenced, while the other X chromosome is packaged as euchromatin and expressed.

      Which brings me back to my original line of inquiry:

      A species may not be able to get rid of its TEs, but a species may adapt to rein in its TEs, which I want to cite as an exaptation of facultative heterochromatin regulation.

      Delete
    28. con't:

      One such adaptation to "rein in" or suppress TE insertional mutagenesis could feasibly be "facultative heterochromatin" formation for those regions of genome whose genes' expression is temporarily not required.

      That means facultative heterochromatin (as just one for example) may subsequently represent an exaptation for higher level gene control that is “exuberantly” redundant.

      This can all occur even (neah - especially) if there was no positive selection at the organism/population level for the build up of the afore-mentioned bulk DNA.

      I realize Barb came up with a great response in an earlier thread:

      bwilson295Tuesday, May 12, 2015 3:42:00 PM

      Seems there are two ways to look at the observation that rearranging junk DNA changes the expression of certain genes. First: The "junk" DNA has a regulatory effect on gene expression. Second: The darn junk DNA interferes with the regulation of gene expression unless it's correctly folded out of the way.

      Distinguishing between those ideas might be difficult; they sort of blend into each other. However, the extremely reduced genomes of fugu and bladderworts lends credence to the second.


      I counter that facultative chromatin does indeed seem to represent the former than the later. In support of my contention I cite the loss of gene control in cancer cells that correlates with loss of facultative heterochromatin control.

      So I counter that Georgi was too quick to dismiss my speculation

      GM There are extremely strong selective pressure to have effective (relatively speaking) mechanisms for silencing TEs. But that's a different subject.

      Delete
  8. Since we're doing analogies today, here's mine.

    Here is what Nessa Carey is saying, almost. Suppose you live in Rhode Island (the smallest US state). You don't want to get cancer, so you move to Texas (which has a much larger population) so that all the Texans there will serve as an insulator protecting you from getting cancer.

    ReplyDelete
    Replies
    1. I wold encourage everyone who thinks like that to move to Texas.

      Delete
    2. They already ... no, better not; Texans are scary.

      Delete
    3. @John: Please reconsider who you award your Nobel to. I deserve to be at least a joint winner, for my comment above making the same point. See comment of Wednesday, May 27, 2015 9:19:00 PM in this thread.

      Sulking ...

      Delete
    4. Woops, it was Nick rather than John who awarded the Nobel.

      Delete
    5. Joe: I deserve a piece of your Nobel in compensation for your error.

      Delete
    6. Joe says: I deserve to be at least a joint winner, for my comment above making the same point. See comment of Wednesday, May 27, 2015 9:19:00 PM in this thread.

      Yes Joe, but I put your comment through several rounds and mutation and selection, producing the more highly evolved, uber-comment.

      You're Rosalind Franklin to my Watson and Crick. By which I mean you're SOL.

      I would like to thank the Academy...

      Delete
  9. Nonexistent Jesus, this book sounds bad. Baaaaad. My condolences, Larry, at the Sisyphean task you have ahead of you to sift through Carey's giant like of sludge.

    ReplyDelete
  10. I agree that in the case of UV, the mutation rate is proportional to the amount of DNA so junk DNA just increases the number of mutations and doesn't protect to functional DNA. This would also apply to DNA Pol errors, but in cases where mutagens are produced by cellular metabolism I think its possible that junk DNA could serve as a decoy, though I think it unlikely this is the case. For one thing I think there are many other molecules; protein and especially RNA that would also react with the same mutagens so having more DNA would have no advantage.
    Has anyone plotted the neutral mutation rate vs genome size to look for correlations?

    ReplyDelete
    Replies
    1. This has been studied extensively. See here for the plots you wanted:

      http://www.ncbi.nlm.nih.gov/pubmed/23077252

      The mutation rate is not just a function of genome size, there are many factors that determine it, including selection. In general, the theoretical expectation is that large effective population size would allow for higher level of optimization of the replication and repair machinery, but it's a bit more complex than that, because one needs to also take into account the total amount of genome space that's under sequence constraints (the more of it, the lower the mutation rate for the same N_e because the selective advantage of any alleles that reduce the mutation rate is higher), etc.

      Delete
    2. the total amount of genome space that's under sequence constraints (the more of it, the lower the mutation rate for the same N_e because the selective advantage of any alleles that reduce the mutation rate is higher)

      If this were true, you could estimate the fraction of the genome that's under sequence constraints (not junk) from N_e and the mutation rate. But that'd be a bit circular because you'd have to assume you know the fraction of genome that's under sequence constraints (not junk) for the example genomes that went into your plot.

      But if you assume you knew fraction of non-junk for a few dozen genomes, you could estimate fraction of non-junk for genomes not yet characterized.

      Delete
    3. Georgi

      I'm far from fluent on this topic but it seems to me the paper you link deals with the mutation rate that we measure from looking at genetic variation in a population. It seems to me that this is distantly connected to the rate of chemical modification of DNA, which we're talking about here. Can you explain?

      Delete
    4. The measurements are mostly from mutational accumulation experiments, i.e. direct measurements

      Delete
  11. This is a useful video for showing the very basics of one of the known biological mechanisms for inducing and controlling mutations that are not errors or accidents they are "guesses":

    Immunology - Adaptive Immunity (B cell Activation, Hypermutation and Class Switching Overview)
    https://www.youtube.com/watch?v=Bl6vWLqL2D0

    ReplyDelete
    Replies
    1. Gary,
      Your use of the word "guesses" implies some sort of conscious agency to the process of somatic hypermutation and B cell affinity maturation. This is not implied at all in the video you link. However, affinity maturation shows in principle how random mutation and natural selection can work, and is evidence against ID creationist claims that random mutation cannot improve protein binding sites.

      Somatic hypermutation of the variable region of antibody binding domains is described very well in the video you linked. The mutations themselves however are random. The B cell is not thinking about what mutations to make and "guessing". The mutations are random. Some mutations make the antibody bind less efficiently to the antigen in question, some improve the interaction, others have no significant effect. B cells with improved binding capacity react with the antigen more frequently and more efficiently and receive proliferation signals more frequently than B cells with poorer binding antibodies. Thus by natural selection the B cells with improved antibody binding out reproduce the inferior B cells.

      Random mutation + natural selection = improved protein binding. This happens billions of times a day across planet Earth.

      Delete
  12. Chris B, you seriously are a scientifically useless (anti)religious zealot.

    You better study this before making an even bigger ass out of yourself, you creep.

    https://sites.google.com/site/theoryofid/home/TheoryOfIntelligentDesign.pdf

    ReplyDelete
    Replies
    1. Gary Gaulin, please educate yourself about intelligent design "theory" before you blurt opinions about it. Ask us; we know more about the "theory" of intelligent design than you do.

      First, there is no theory of intelligent design, according to ID proponents.

      Paul Nelson, ID proponent, 2004: "Easily the biggest challenge facing the ID community is to develop a full-fledged theory of biological design. We don't have such a theory right now, and that's a real problem." quoted on page 64 of "Interview: The Measure of Design, A Conversation About the Past, Present & Future of Darwinism & Design". Touchstone 17 (6): 60–65. July–August 2004.

      ID can't make testable predictions. Both William Dembski and Stephen Meyer said in the 1990's that ID can't make predictions. Meyer later contradicted this statement and made lists of fake predictions that don't logically follow from the ID hypothesis (such as, no Junk DNA.)

      The mutations you spoke of are random, not "guesses."

      Delete
    2. All who have been throwing religiously loaded insults instead of helping to scientifically explain the origin of intelligence are scientifically lazy hypocrites, promoting a religious agenda of their own, instead of being interested in finding scientific reason.

      Delete
    3. Well, Gary, that was a creative and entirely false ad hominem attack, Of course, it failed entirely to address any of the content of my posts in this thread. So let's hear it, Gary, explain how my scientific explanations here are wrong. My post on affinity maturation contained no religious references at all. And what does this have to do with the 'origin of intelligence"?

      Delete
    4. The way the scam works is to only allow their favorite strawmen (Dembski, Behe, etc..) to speak for the scientific merits of a theory premised to explain "intelligent cause". At the same time someone who codes applicable computer models and has adequate experience in cognitive science are totally ignored while their crowd keeps ramble on about the importance of getting expert opinions instead of listening to Dembski, Behe, etc..

      I have never in my life ever seen this much hypocrisy. The money-pits that are taking advantage of the situation have vested interests in keeping the scam going, forever.

      Delete
    5. Gary, you yourself have been "throwing religiously loaded insults" in almost every comment you write. You constantly drag religion into every thread and every sub-thread, based on your false equivalence that "Darwinism" is a religion.

      Gary Gaulin: Chris B, you seriously are a scientifically useless (anti)religious zealot.

      ...scientifically lazy hypocrites, promoting a religious agenda of their own

      I tire of your relentless use of religion as a substitute for evidence and testable hypotheses and your endless name-calling while hypocritically accusing others of name-calling.

      "instead of helping to scientifically explain the origin of intelligence"

      Gary, you have done nothing to explain the origin of intelligence. You merely allege a cause without evidence. Allegations of cause are not necessarily explanations. To count as scientific explanations, they must either 1. be deductions from generally observed principles or 2. lead to unusual, distinctive, predicted observable phenomena that match observations.

      You never did either. You are what I call a "definitional crackpot", someone who gives idiosyncratic definitions of words and then insists that his definitions have to be treated as if empirically proven. Thus you claim human intelligence is based on "cellular intelligence" which is based on "molecular intelligence" etc., defining a bunch of terms that no one gives a shit about, and that you can't get into the peer-reviewed literature, because you have never demonstrated that such definitions are an essential part of a theory that makes testable predictions about observable phenomena.

      Yet you insist upon acting as if your definitions have the status of empirical observations.

      An allegation of cause unsupported by evidence is not an explanation. You have no explanation, and you have contributed nothing to "cognitive science", and none of us here give a shit about cognitive science anyway.

      The question is affinity maturation in the immune system. That is based on random mutations, not "guesses". When you called them "guesses" you were lying.

      Delete
    6. And Gary Gaulin launches the Appeal to Motive Fallacy:

      I have never in my life ever seen this much hypocrisy. The money-pits that are taking advantage of the situation have vested interests in keeping the scam going,

      So, still no explanation for the origin of intelligence. Just alleged appeals to his vast knowledge of other people's motives. C. S. Lewis called this fallacy Bulverism; I call those who apply it motivities.

      Every right-wing dispute nowadays boils down to Appeal to Motive. How can you disprove the evidence for global warming? "The climate scientists are in it for the millions and millions of dollars in research money!" $%^& you, I have zero tolerance for motivites.

      We can rebut Appeal to Motive with Appeal to Motive: you're trying to discredit real science because you want some of the right-wing think tank gravy train $$.

      Delete
    7. "Gary, explain how my scientific explanations here are wrong."

      I am not going to chase your red-herrings in circles until I drop dead from exhaustion.

      It's you who have some explaining to do:

      http://theoryofid.blogspot.com/

      If you have a problem with that model then you are expected to provide a better scientific model for explaining how "intelligent cause" works at all levels of biology that can possibly be intelligent.

      Delete
    8. "I am not going to chase your red-herrings in circles until I drop dead from exhaustion.

      It's you who have some explaining to do:

      http://theoryofid.blogspot.com/

      If you have a problem with that model then you are expected to provide a better scientific model for explaining how "intelligent cause" works at all levels of biology that can possibly be intelligent. "

      What an amazing piece of projection that was, Gary. It tops even your vicious attack earlier in the thread wherein you label my (admittedly bare-bones) description of affinity maturation in B cells as antireligious zealotry. (?!)

      I gave a one paragraph summary of the current state of the art science on affinity maturation, not a red herring. It is the culmination of decades of painstaking work by immunologists, cell biologists, biochemists, geneticists, and scientists from a handful of other disciplines. They worked their asses off to assemble a descriptive, predictive model of how affinity maturation of B cells works, and the work continues. If you want to replace it with YOUR model, then it is YOU who has some explaining to do. Provide your one paragraph summary of the model you want to replace it with, and explain how it fits the data better than my description. That's how science works. Don't send me off to red herring websites.

      In addition, I don't need to provide you with a better scientific model for "intelligent cause". You have yet to provide evidence that "intelligent cause" has anything to do with affinity maturation or any other naturally observed phenomena. I am not going to chase that red herring in circles.

      Delete
    9. Yes, Gary, you should recognize that what you have here is not a theory, but an idea. There is a big difference. Your idea appears to be that, what others call molecular and cellular effects and characteristics, you call intelligence. That is your idea. And forgive people for being suspicious that the whole goal of this idea is to ask: from where does molecular intelligence emerge? We already know what your answer to that question is, and that it is intended to be the answer to end all further questions.

      Delete
    10. SRM: Your idea appears to be that, what others call molecular and cellular effects and characteristics, you call intelligence. That is your idea.

      Nailed. Stick a fork in him, he's done.

      I'd like to see Gary try this shit at a scientific conference in front of real scientists.

      I'm going to call molecular effects "molecular intelligence." And I'm going to call cellular effects "cellular intelligence." That explains where intelligence comes from. If you don't agree this is empirically proven, you're a religious zealot motivated by greed and part of the "money pits" with a vested interest in keeping the scam going. Stop your nane-calling, religious freak!

      Yeah that'd go over big. It's a wonder it hasn't caught on already.

      Delete
    11. "If you don't agree this is empirically proven, you're a religious zealot motivated by greed and part of the "money pits" with a vested interest in keeping the scam going."

      I've been a scientist for a while now, and you know what, I didn't get into it because of greed. I know, pick your mandibles up off the floor, but I didn't choose science for the $$$$, cars and fabulous babes. I have yet to see the "money pit". Maybe you have to be twenty years out of graduate school before you are invited into the "scam"?

      Delete
    12. This is an example of what has been labeled as religion then thrown out of science by those who claim to be science defenders:

      Ask any roboticist of a certain age, whether a professional or hobbyist, how they first got interested in robots. Odds are good they'll mention a 1976 TAB book, written by David L. Heiserman, called Build Your Own Working Robot. The book described the construction of Buster, a small, wheeled robot. This was before the era of ubiquitous microprocessors. Buster's brain was a mass of TTL logic chips that implemented surprisingly complex behaviours. In some ways, Buster was not unlike Grey Walter's vacuum tube-based turtle robots from the late 1940s and was likely the first significant step forward in behavior-based robots since Walter's turtles. Did you ever wonder what Dave did after writing those books or what he's up to today? Read on to find out!

      Two years after Build Your Own Working Robot was published, Dave Heiserman returned with another robot book that brought behaviour-based robots into the computer age. The new book, called How to Build Your Own Self-Programming Robot, described the construction of Rodney. Starting with no knowledge, Rodney explored and learned about his world through trial-and-error, using what he learned to anticipate future explorations.

      All of this behaviour-based robotics stuff was considered a bit kooky by mainstream researchers in the 1970s, who favored top-down strong AI. Why bother building little insect-level robots that puttered around on the floor? Machines needed to understand deep philosophical questions first. They needed to represent the entire world symbolically and reason about it like human brains. Only then would we be ready to put them on wheels or legs. So even though hobbyists almost immediately set to work building Buster clones, Heiserman was largely ignored elsewhere. But mainstream AI was already running into dead ends, entering what's now known as the AI Winter. And those Buster-building hobbyists were entering Universities and beginning to set the stage for a change in the direction of AI research. Before long, Rodney Brooks arrived on scene and coined the name 'subsumption architecture' to describe his own bottom-up, behaviour-based robots. Robotics and AI research were revitalized.

      While you aren't likely to see a mention of Heiserman in any official history of AI or robotics, it hard to imagine that his books didn't play a part in those changes. Even today I find that most hobby roboticists still remember him. Many still have the two books shown above or one of his many other books. I was reminded of this recently when, during a visit the Dallas Personal Robotics Group, I ran across several copies of Build Your Own Working Robot in the group's library. I picked one up, opened it, and realized it was the very copy that I had bought in 1976 and later donated to the DPRG. It got me thinking about all of this and I wondered whether Dave might still be around. I set out to find him and, along the way, I collected questions from other robot builders; questions they'd always wanted to ask the author whose books inspired their interest in robotics. I did find Dave and he graciously agreed to an interview. Below you'll find his answers to your questions.


      http://robots.net/article/3428.html

      Delete
    13. Gary, you're lying. No one has labelled the above "religion".

      This is an example of what has been labeled as religion

      You're lying. You cannot link to a single example of anyone labeling that "religion."

      then thrown out of science

      The above passage is not science. It is a memoir. Arguably, it is relevant to history of science. But it can't be thrown out of science because it was not science to begin with.

      Ad hominems, name-calling and appeal to motive is all you've got.

      Delete
    14. You do understand AI is a thriving scientific discipline, and not at all dismissed as "religion". That characterization just doesn't square with reality.

      http://www.sciencedaily.com/news/computers_math/artificial_intelligence/

      Delete
    15. Maybe you have to be twenty years out of graduate school before you are invited into the "scam"?

      No. It's better to be less than twenty years out of graduate school and too naive to realize that you are involved in a very sinister scam.

      Delete
    16. Gary, you're lying. No one has labelled the above "religion".

      Your dishonest responses above indicate that you are simply trashing science that does not serve your unscientific agenda.

      Delete
    17. You do understand AI is a thriving scientific discipline,

      When I was growing up the promise of AI was that by the year 2000 we would all have a robot to do our house chores for us. These days the ultimate goal of AI research has been downsized to animatron sex-bots that do not have the intelligence to demand a lifetime commitment or can say "No!".

      Delete
    18. Your dishonest responses above indicate that you are simply trashing science that does not serve your unscientific agenda.

      Well, you probably wasted enough of everyone's time, Gary. Your comment above is not even projection, it is simple-minded mimickry of what is obviously an honest and devestatingly accurate criticism of creationism. Mimic is what nearly all the creationists here do and that is very telling.

      Delete
    19. "Your comment above is not even projection, it is simple-minded mimickry of what is obviously an honest and devestatingly accurate criticism of creationism."

      Yes I already know that your only concern is your religious agenda, which judges the scientific usefulness of scientific theories by which ideology they most serve.

      Delete
    20. Chris B,

      "You do understand AI is a thriving scientific discipline, and not at all dismissed as "religion". That characterization just doesn't square with reality."

      You do understand that Gary sent you after a red-herring, right?

      Delete
    21. Well, a red-herring, and he wanted you to understand that he is a poor mischaracterized scientist. One who is laughed at because others just can't understand his amazingly intelligent ideas and scientific insights. He is the new Galileo. The new Copernicus. The new Newton. The new Darwin. The new Crick. The new Paulin. Only you still don't know too busy with your "old models." Gary thinks that our laughing at him is a reflection of his great insight, not of his stupidity.

      Of course, my answer to Gary would be what Carl Sagan said:

      "They laughed at Columbus, they laughed at Fulton, they laughed at the Wright brothers. But they also laughed at Bozo the Clown."

      Delete
    22. You do understand that Gary sent you after a red-herring, right?

      Only if you consider "thriving" to mean getting millions of dollars in AI funding to write Darwinian based junk that cannot even explain how intelligence works.

      The joke's on you.

      Delete
    23. photosynthesis,

      Instead of defending his ideas in a coherent, concise manner, Gary has decided that either long paragraphs of word salad or terse instructions to visit web sites substitute for science.

      When he describes science as a big scam (that we are all just too naive to fathom), that things like affinity maturation of B cells are part of a religious agenda (while earlier accusing me of being an antireligious zealot), and that AI research is a bunch of "Darwinian based junk", he's on his own. I'll not waste any more time indulging Gary in his conspiracy theories and mental pathology.

      Delete
    24. When he describes science as a big scam

      Now comes the tactic of shoving words in my mouth, while acting sincere.

      Delete
    25. Gary, you are mistaking this for a creationist or ID site, where "tactics" are always employed and applauded. Just like your tactic of parroting the legitimate criticisms made by scientists against ID, because you have no actual scientifically valid criticisms against evolution. You should spend your time at UD where you will be admired by people who know little about science.

      Delete
    26. I made it clear that forcing personal religious interpretations of cognitive science information that uses words like "guesses" and "intelligence" is a religious practice that is very out of bounds of science. In US classrooms it's not even constitutional. A science teacher or school committee could end up in court for preaching that and probably badly lose, like the other side of the extreme did in Dover.

      Some may not know it but they got themselves stuck in a very bad situation, which was caused by religious extremisim getting out of control. There is no constructive discussion, just constant changing of the subject from models to demonstrate the basics of how intelligence works to something else by throwing insults or chanting the usual mutation and selection did-it answers along with praise to EA's that supposedly already revealed all of that and any who deny that deserves well funded punishment meant to destroy them that even promotes public school curriculum stereotyping their work too as religious pseudoscience.

      Delete
    27. SRM,

      You are wasting your time. Gary has no intention of being honest. He has the hubris (or maybe he doesn't even realize he is doing it) to say:

      "When he describes science as a big scam

      Now comes the tactic of shoving words in my mouth, while acting sincere."

      in the very same thread that he said:

      "I have never in my life ever seen this much hypocrisy. The money-pits that are taking advantage of the situation have vested interests in keeping the scam going, forever. "

      and

      "No. It's better to be less than twenty years out of graduate school and too naive to realize that you are involved in a very sinister scam. "

      And he accuses me of being insincere and shoving words in his mouth. There is just no reasoning with that. You are right, his style of "debate" is well suited UD.

      Delete
    28. SRM,

      Gary also says:

      "I made it clear that forcing personal religious interpretations of cognitive science information that uses words like "guesses" and "intelligence" is a religious practice that is very out of bounds of science. In US classrooms it's not even constitutional."

      Yet this whole row started when Gary said this:

      "This is a useful video for showing the very basics of one of the known biological mechanisms for inducing and controlling mutations that are not errors or accidents they are "guesses":"

      I objected that the video neither said nor implied anything about 'guesses', which suggests a conscious agency, but that the mechanism of affinity maturation of B-cells uses random mutation + selection for better binding antibodies. Gary then called me an antireligious zealot, and the conversation circled the drain from there.

      Delete
    29. Since when does the phrase "The money-pits that are taking advantage of the situation" equal the word "science"?

      The money-pits that are taking advantage of the situation are no friend of science, and very few scientists who knew the details would even take them seriously. This is about paid science administrators who use their power to promote religious agendas. And wasting money on politically correct junk that is already scientifically obsolete or is not even science to begin with.

      Delete
    30. Not surprising that a few observations may just counter-act the assertion of a ID supporter...

      1) You truly underestimate the average scientist's love of a good old paradigm shift, and a chance to immortalize their names in the textbooks. If Behe et al actually had a killer idea, your would see everyone flocking to to it early, to get their name in for the Nobel discussions. Look at the current CAS/CRISPR frenzy.

      2) the "money-pits" of science at the moment are throwing the money at the mega-data based projects. Ones that ID'ers seem to promote quite a lot, like ENCODE. Not really consistent with a conspiracy.

      3) The head of one of said money pits - Francis Collins - seems to have a "religious agenda" of the more Evangelical Christian variety, and is putting it into books.

      What is your point again, other than ad hominem slandering?

      Delete
    31. 3) The head of one of said money pits - Francis Collins - seems to have a "religious agenda" of the more Evangelical Christian variety, and is putting it into books.

      Was I supposed to disagree?
      BioLogos is one of the best examples of them all. And I expect that they want nothing to do with me!

      Delete
    32. Gary: BioLogos is one of the best examples of them all.

      Examples of what? Money pits? Please compare the income of Biologos to that of the Discovery Institute, Answers in Genesis, the Creation Museum and the Ark Park.

      The Discovery Institute makes > $5 million a year. That's a lot more than Biologos, I believe. So you must admit that Intelligent Design is a well-funded, religiously motivated money pit that suppresses criticism of its doctrine and tolerates no comments or criticism on its web pages.

      The DI promotes ENCODE which was funded to the tune of $300 million. Talk about a money pit.

      Meanwhile, Ken Ham is shitting bricks over a $15 million tax break he lost for his Ark Park because he won't employ Jews or non-Christians. Talk about a money pit.

      There's a lot of money in anti-Darwinism, but no dissent or criticism is allowed. Ken has a book...

      But returning to our topic, Gary, why did you link to a video about affinity maturation and claim it was about how random mutations are "guesses" which you presumably believe are products of "cellular intelligence"? The video said no such thing, and the mutations are still random. Can you please continue your policy of screaming "Religious motivations! Religious ZEALOT!!" every time you can't provide evidence to back up your bizarre assertions about intelligent cells "guessing"?

      Appeal to motive, appeal to motive, appeal to motive. No answers, no evidence, no sense, just appeal to motive. Religiously motivated appeal to motive, dare I say.

      Delete
    33. Gary bitterly complains: The money-pits that are taking afvantage of the situation are no friend of science, and very few scientists who knew the details would even take them seriously. This is about paid science administrators who use their power to promote religious agendas. And wasting money on politically correct junk that is already scientifically obsolete

      Now now, Gary. Just because you don't understand its function doesn't mean it's junk!

      Delete
    34. P.S. "Politically correct junk" = ENCODE. Biggest "religiously motivated money pit" there is.

      Delete
    35. P.S. "Politically correct junk" = ENCODE. Biggest "religiously motivated money pit" there is.

      I have needed their data for my own research work. It's the only place around for details that show what I needed to see.

      And I have nothing against Francis Collins, I admire him as a scientist and think BioLogos has been somewhat useful to others. The problem is that they promote ID stereotypes that attack my credibility while the Templeton Foundation only funds corporate interests that find it necessary to help ruin my life for entirely religious reasons, while science (answers questions by explaining how things work or happened) gets to go to hell in the religious crossfire.

      Delete
    36. Gary, way to not answer any of my questions. So far in this thread you've

      1. Said affinity maturation is due to cells "guessing" not random mutations, presenting as evidence a video that said no such thing. When challenged to present better evidence, began screaming about religion

      2. Copied and pasted a long, inoffensive passage about robotics and said that passage was dismissed as religious twaddle. When asked who, where, when dismissed this passage as religious twaddle, you ditched the subject and screamed about religion.

      3. Complained about religiously motivated "money pits" that suppress dissent. When asked if the Discovery Institute and Ken Ham's Ark Park are religiously motivated "money pits" that suppress dissent, you ditch the subject and complain about Biologos, a "pit" with far less money than its creationist rivals, and one that does not suppress criticism, unlike anti-Darwinists who tolerate no dissent.

      You can't defend a single thing you write. Now change the subject and Gish Gallop away.

      Delete
    37. Diogenes you just changed the subject. I was explaining the proper terminology for cognitive science (i.e. David Heiserman above).

      Delete
    38. I wrote: You can't defend a single thing you write. Now change the subject

      Gary Gaulin responded: Diogenes you just changed the subject.

      As SRM already stated, so appropriately, above: "Well, you probably wasted enough of everyone's time, Gary. Your comment above is not even projection, it is simple-minded mimickry of what is obviously an honest and devestatingly accurate criticism of creationism. Mimic is what nearly all the creationists here do"

      Delete
    39. Then both of you (and several others) need professional help with your issues, before you get yourselves into even deeper trouble from posting insane garbage like that.

      Delete
  13. The idea isn't completely stupid.

    As many many people have pointed out, the idea does *not* make sense for mutation processes that occur at a constant rate u per bp. In that case, the "insulator" or "decoy" idea is like building trailer parks around a city to serve as decoys for the tornados.

    However, the idea *might* make sense if there is a limited source of damage or mutations that could be absorbed. Then the junk DNA could serve as a decoy or insulator. X-rays mostly pass right through your soft tissue, so the idea that junk DNA would be serving as a decoy to absorb x-rays would be a non-starter. Now, if an organism grew extra-big bones, or lead shielding, then this might protect against xrays reaching the gametes.

    Free radicals and UV are constantly causing damage to DNA and proteins. Repair of damage to DNA is happening millions of times per cell per day in your skin cells. There is presumably an equilibrium level of damage based on the balance of damage and repair. Having more DNA doesn't necessarily change that, because adding more DNA dilutes the damage at the same time it is diluting the repair.

    In the case of insertion elements, then the idea is more plausible, but still problematic. The rate of insertion is a function of the number of source elements, not the number of target sites. So if you increase the number of target sites, this dilutes the rate of insertion per site.

    But the process back-fires, because the larger genome eventually gets more elements.

    There might be some other circumstance i which it would work.

    So, as I say, the idea isn't completely stupid. It's just *mostly* stupid.

    ReplyDelete
    Replies
    1. Arlin; Friday, May 29, 2015 4:26:00 PM:

      "However, the idea *might* make sense if there is a limited source of damage or mutations that could be absorbed. Then the junk DNA could serve as a decoy or insulator"

      Arlin,

      I wondered when will you intervene in our discussion here at Sandwalk about the so called 'junk DNA' (jDNA), and elaborate on it in the context of your *constructive neutral evolution concept*.

      I don't know what references Carey cited in support of the idea that jDNA might serve as buffer against mutations and against cancer, but this is the idea behind my theory that I proposed 25 years ago to explain the C-value paradox and the biological function of jDNA (http://www.ncbi.nlm.nih.gov/pubmed/2156137 ; http://biorxiv.org/content/early/2013/11/18/000588).

      As several people here at Sandwalk, including you and I, have pointed out, the rational behind buffering idea as presented by Carey is obviously flawed. However, you made the point that if the mutagen is in 'limited supply', then the idea could be interesting, and you mentioned "insertion elements."

      Then, you undermined my theory by saying that, "the process back-fires, because the larger genome eventually gets more elements (BTW, Joe Felsenstein has made a similar argument against my hypothesis a while ago).

      Doesn't this argument undermine your own *constructive neutral evolution concept*?

      Delete
    2. Sorry, what I said was not clear. The process "backfires" in the sense that the added DNA becomes a refuge for more insertion elements, which increases the total genomic rate of insertion. The problem in biochemical terms is that the extra DNA is also a "decoy" for DNA-binding proteins. Adding more DNA will suck away a portion of every protein due to non-specific interactions. Adding more DNA will increase nuclear volume. The significance of this is that many elements have a genomic frequency that reflects a negative feedback loop based on regulatory repression. For such elements, doubling the genome size will lead to a burst of transposition until the original genomic density is restored.

      But those are arguments about the *equilibrium* effect, where we imagine adding extra DNA and then letting the system go to equilibrium.

      If instead the system *just keeps adding extra DNA and never reaches equilibrium*, then there could be a perpetual buffering effect. One would have to work out the exact dynamics to know how this idea could ever make sense.

      If you have been working on this idea for 25 years, and you haven't worked out the dynamics, then I suggest that you do that. A rigorous model that works will be the best way to convince people to pay attention to your idea.

      I don't see any relationship to constructive neutral evolution. Perhaps you could explain what you mean by that.

      Delete
    3. Hi Arlin,

      I also have to say sorry, as what I wrote was not too clear.

      I think, I understood your argument that having a 'safe-haven' for the accumulation of new inserting elements might, in fact, 'back*fire*' by introducing new potential inserting elements, which might undermine the very protective function I was trying to make the case for.

      Ironically, in my recent paper, I metaphorically referred to the putative protective function of jDNA as a classic case of fighting *fire* with *fire*. Well, as some people would say, when you play with *fire* you might get burn.

      However, I don't think that is the case with the model I proposed for the evolution of genome size and the biological function of the so called jDNA, which is a good example of what you might call "constructive neutral evolution". I don't know if you had the chance to read my papers, but I think the evidence and arguments I present in support of my model make it a candidate for a good example of "constructive neutral evolution.' If, after reading the paper, you still maintain that you don't see any relationship, I'll try to elaborate on it.

      If you read my papers, you'll also realize that I specifically addressed the 'nucleotypic effects' that you are eluting to, but from a different perspective (BTW, you can find the text of the original paper in the "Data Supplements" of the bioRxiv paper; http://biorxiv.org/content/biorxiv/suppl/2013/11/21/000588.DC1/000588-1.pdf)

      Regarding your suggestion that I should have developed my model on the origin and evolution of genome size and C-value paradox or enigma, you are right, I should have put more effort into developing and promoting it. However, modeling this theory is relatively complex, because the model also includes the "somatic dimension" of inserting mutagenesis, particularly by exogenous retroviral elements, leading to cancer. It's a rather complex situation that must rely on many 'assumptions' that are difficult to define even now when our understanding of dynamics of endogenous and exogenous inserting elements and the biology of neoplastic transformation has improved.

      Delete
    4. Arlin,

      You might not get around to read my paper, so I thought of posting here an excerpt that might resonate with you:

      "One of the most bizarre, but highly intriguing genome defense systems against invading inserting elements is found in ciliates, a highly diverse group of protozoans [29]. These organisms have two genomes: a germ-line, diploid genome, which is transcriptionally silent and carries tens of thousands of mobile elements, and a transcriptionally active polyploid genome, which originates from the germ-line genome by programmed DNA rearrangement and elimination of mobile elements. In some groups of ciliates, such as Oxytricha, over 90% of the germ-line genome is composed of jDNA, which is eliminated during the programmed DNA deletion. Apparently, in these single-cell organisms, maintaining the jDNA as a defense system against insertional mutagenesis in the germ-line genome was under very strong positive selection."

      You have used the evolution of scrambled ciliate genes and a 'textbook' example of constructive neutral evolution. As shown in the excerpt above, I consider the genome rearrangement in ciliates a 'textbook' case of genomic defense systems against inserting elements.

      What do you think?

      Delete
    5. Claudiu, the request is the same as it has always been - show us the selection coefficients.

      If you can't then there is no point continuing conversation any further

      Delete
    6. Yes, we have discussed this, but let's hear other people's opinion. However, perhaps, you should also ask Arlin about "selection coefficients" in his examples of constructive neutral evolution; -:)

      Delete
    7. Hi Claudiu,

      I just occurred to me

      TE mutagenesis = indel events and the majority of indel events can be classified as proximal and in cis (forgive such outdated and out of fashion terminology) even though a minority of TE events can occur in trans (for lack of a better term)!

      In other words - if an organism cannot completely eliminate or purge the genome of TEs then the next best thing is to isolate the TEs with surrounding genomic buffers.

      I am probably merely restating what you already made clear but did not manage to penetrate my Teutonic cranium. Thinking of your model along such lines made it suddenly clearer to me.

      I hope I am not guilty of cerebral flatulence just now.

      Delete
    8. TEs can also result in inversions and deletions - proximal events in cis as well as tandem repeats yet another proximal event in cis... and of course transposition.

      But let's focus on the negative consequences of inversions and deletions for the time being:

      As mentioned above, the suppresion of TE insertional mutagenesis could feasibly be "facultative heterochromatin" formation for those regions of genome whose genes' expression is temporarily not required.

      That means facultative heterochromatin (as just one for example) may subsequently represent an exaptation for higher level gene control that is “exuberantly” redundant.

      And why not, the loss of gene control in cancer cells that correlates with loss of facultative heterochromatin control.

      Making me wonder if Georgi is being patently unfair:

      the request is the same as it has always been - show us the selection coefficients.

      Which selection coefficients?

      When control breaks down, selection at the level of selfish DNA takes over. Meanwhile, if I understand you correctly, the fixation of this higher and exuberantly redundant level of control would presumably be at a higher order of selection - I presume you are thinking about selection at the "species level", which again would render Georgi's challenge "unfair".

      Still Georgi does have a point about the burden of proof resting on your side.

      How best to resolve this impasse?

      Delete
    9. Claudiu BandeaTuesday, June 02, 2015 9:45:00 PM
      Yes, we have discussed this, but let's hear other people's opinion. However, perhaps, you should also ask Arlin about "selection coefficients" in his examples of constructive neutral evolution; -:)


      Nice evasion.

      However, he is not claiming that something is a selected effect, i.e. he is working under the null model. You are rejecting the null model. Do you see the difference?

      Delete
    10. Tom MuellerTuesday, June 02, 2015 10:41:00 PM

      Which selection coefficients?


      The ones associated with the insertion or deletion of a piece of DNA of given length under the models proposed to explain the presence of all that extra DNA as being beneficial.

      BTW, he does not even have to do that - I have done it for him on several occasions in these comments. He just have to acknowledge the fact that this has to be given some attention and then think about it.

      Delete
    11. Tom,

      As I stated before, the points your made, including those related to the Peter Fraser’s work on chromatin dynamics, are highly relevant.

      For example, you wrote:

      As mentioned above, the suppresion of TE insertional mutagenesis could feasibly be "facultative heterochromatin" formation for those regions of genome whose genes' expression is temporarily not required. That means facultative heterochromatin (as just one for example) may subsequently represent an exaptation for higher level gene control that is “exuberantly” redundant.

      These are great insights into the extraordinary "selective pressure" associated with transposable and viral elements and on how the host respond to them by adapting to their presence and by using their components and mechanisms (through exaptation) not only as defense systems, but also in other cellular processes (e.g. use of micro-RNAs for gene regulation).

      Delete
    12. Georgi Marinov, Wednesday, June 03, 2015 12:50:00 AM

      "Which selection coefficients?

      The ones associated with the insertion or deletion of a piece of DNA of given length under the models proposed to explain the presence of all that extra DNA as being beneficial.


      In the context of my model on the evolution of genome size and the biological function of the so-called "junk DNA" (jDNA), a DNA fragment of a few hundred or even a few thousands base pairs has a protective function only if added to the other thousands of jDNA fragments in the genome. You can think about it as "the whole is greater than the sum of its parts."

      Regarding the question: "so, how did the jDNA get there to begin with?", you might want to think in terms of 'neutral evolution', or, even better, read some of Arlin's inspiring papers on "constructive neutral evolution" and "new-age mutationism":

      http://www.ncbi.nlm.nih.gov/pubmed/10441669
      http://www.ncbi.nlm.nih.gov/pubmed/19625453
      http://www.ncbi.nlm.nih.gov/pubmed/23062217

      Delete
    13. Regarding the question: "so, how did the jDNA get there to begin with?", you might want to think in terms of 'neutral evolution', or, even better, read some of Arlin's inspiring papers on "constructive neutral evolution" and "new-age mutationism":

      OK, so basically this is conclusive evidence that I should stop wasting my time responding to you

      Delete
    14. Hi Claudiu

      Let’s connect some dots:

      You are conjuring up long forgotten memories. That said, I am hopelessly out of date.

      I am delighted that some quick google-whacking confirms some old-fashioned notions are back in vogue again today.

      Genome instability in cancer includes chromosomal translocations, chromosomal inversions, chromosome deletions etc (sound familiar?)

      It gets better – it appears that Heterochromatin dysregulation has everything to do with Genome instability and "cancer progression".

      Raising an intriguing question: How does one measure selection coefficients for epigenetic phenomena?

      At this point I am wary to proceed, since we are treading into the domain of Epigenetics, and I fear the provocation of Larry’s ire on subjects already rehashed before.

      http://sandwalk.blogspot.ca/2014/03/what-is-epigenetics.html

      Delete
    15. Hi Georgi

      We just cross-posted,

      re your response to Claudiu

      OK, so basically this is conclusive evidence that I should stop wasting my time responding to you...

      OK - clearly I am out of my depth and I must have missed something. What's up? I did not understand what motivated your response. I was thinking that Claudiu perhaps may be on to something.

      What am I missing besides the the salient point the burden of proof is on his side which is how I interpret your demands for selection coefficients?

      Delete
    16. What you're missing is all the times I have explained those things to him in the past, which should have made it abundantly clear, beyond any reasonable doubt, that I happen to not be completely ignorant of what neutral evolution is. Yet you saw the content his last post...

      So what is the point of explaining it again?

      Delete
    17. @ Georgi

      re:
      "so, how did the jDNA get there to begin with?"

      I answered that above
      http://tinyurl.com/pqw2fdd

      The sadly mismonikered "selfish DNA" aka parasitic DNA jumps to mind.

      This would be at a different level of selection.

      Of course at some point, a species would need to evolve to rein in its TEs.

      I never felt you provided a complete response to that question of mine to you.

      Delete
    18. Georgi

      How Ironic is this - I am a typical German with with the social graces of a typical German which is very sad indeed and yet I am thrust into the role of conciliator.

      May I suggest that you and Claudiu both speak English as a second language and perchance at times misspeak and/or are misunderstood.

      I am willing to bet that if we wee all to sit down together at a table over a few shots of schnaps, our discourse would be far more congenial.

      Now there is an idea!

      Delete
    19. Quite the opposite - I did provide an explanation.

      For something to be an exaptation, it needs to be maintained by purifying selection. Otherwise it's no different from neutral sequences and you can't claim it has a "function"

      So the same observation that kills the argument that the "jDNA" was accumulated through selection (because the selective advantage of insertion of additional DNA is too small to be visible to selection, therefore the null model - neutrality - has not been rejected) kills the idea that it got there by neutral means but now it has acquired the function of protecting the genome. The selective disadvantage of deletion is too small for it to be visible to selection, i.e. it is not actively maintained by selection, and therefore the null has not been rejected. This is under the buffering against TE insertion/regulation of nuclear volume/cells size/etc. models

      You can handwave that the extra DNA is now there because CNE-like mechanisms resulted in the spacing between regulatory elements being fixed, and now it cannot be disrupted. But this is more of a pure conjecture with no solid body of evidence to support it at this moment (if a good set of a very large number of genomes with large indels annotated as well as well matched biologically RNA-seq samples for those becomes available, we may be able to test it; the other way is experimental, which will become more feasible in the future, but the former is preferable because it's cheaper as those datasets will be generated for other purposes - this hypothesis does not warrant spending too much money on it at the moment).

      Delete
    20. Well, on this particular thread, I was having a conversation with Arlin, and your jumped into it. Nevertheless, I agree that you should not waist your time responding to me; you'll be better off reading papers, such as Arlin's papers that I suggested above.

      Delete
    21. This comment has been removed by the author.

      Delete
    22. Claudiu - I refer you to (Ecclesiastes 3:1-8) and failing that to Pete Seeger's The Bitter and the Sweet album and the song Turn Turn Turn...

      There is a time and place for everything - including scoring debating points.

      Of course nobody does that better than Diogenes of Sinopian fame and his targets more than deserve his opprobrium... but as as gentlemen discoursing amongst each other; different rules of engagement should come to play when earnestly debating matters of gravitas.

      I have an ulterior motive at play here: I have some unresolved questions that continue to perplex me and I regret to see that anger and indignation has gotten in the way of an exchange that would enlighten me.

      Claudiu - I think you have been the target of the occasional rhetorical debating point and I can understand your vexation.

      That said - I think you just passed up the perfect opportunity to reboot the exchange between you & Georgi who I think has demonstrated gentlemanly patience.

      Dammit all: I wish I could sit down with you two over a couple shots of schnaps and in gemütlich fashion resolve this question once and for all in friendly fashion!

      Delete
    23. @ Georgi

      re:

      For something to be an exaptation, it needs to be maintained by purifying selection. Otherwise it's no different from neutral sequences and you can't claim it has a "function"

      This is where you lose me... why does parasitic DNA need to be maintained by purifying selection at the level of the host?

      I understand from a host's POV, the parasitic DNA represents from the host's POV negative selection at worst (when deleterious), neutral at best if the parasitic DNA remains innocuous enough. However from the POV of the parasitic DNA, propagation and concomitant genome expansion represents an instance successful parasitic DNA expansion subject to positive selection at a level different than the host. OK OK I admit that Gould phrased it better than I.

      To suggest that the host must eventually evolve defensive responses to rein in the parasitic DNA only means we have shifted our focus (at a later point in time) to the level of the host where parasite propagation within the genome is no longer innocuous (neutral) requiring the eventual mechanism for protection of the genome.

      A species may not be able to get rid of its TEs, but a species may adapt to rein in its TEs.

      One such adaptation to "rein in" or suppress TE insertional mutagenesis could feasibly be "facultative heterochromatin" formation for those regions of genome whose genes' expression is temporarily not required.

      That means facultative heterochromatin (as just one for example) may originally have evolved as defense against TE mutagenesis, subsequently represents an exaptation for higher level gene control that is “exuberantly” redundant. On an earlier occasion it was even suggested that the host had co-opted parasitic DNA into a synergistic relationship.

      This can all occur even (neah - especially) if there was no positive selection at the organism/population level for the build up of the fore-mentioned bulk DNA.

      I realize this line of reasoning smells duplicitous - we are shifting horses in mid-stream as it were, but in fact that is exactly the line of reasoning required when parasitic DNA expansion is no longer innocuous and becomes a deleterious burden.

      Forgive my clumsiness in attempting phrase my thoughts.

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    24. OK - it is past my bed time and I realize that last post was a bit garbled...

      ... will return tomorrow.

      best regards to one and all - especially Diogenes. It has been decades since Houston Stewart Chamberlain crossed my radar.

      Delete
    25. This is where you lose me... why does parasitic DNA need to be maintained by purifying selection at the level of the host?

      But I have never said anything of the sort???

      To suggest that the host must eventually evolve defensive responses to rein in the parasitic DNA only means we have shifted our focus (at a later point in time) to the level of the host where parasite propagation within the genome is no longer innocuous (neutral) requiring the eventual mechanism for protection of the genome.

      That's not how it worked - the mechanisms were already there. Pretty much all eukaryotes share them, including the ones with compact genomes. There wasn't really an evolution of defense mechanisms at a later time points. It's the efficiency of selection that changed over time (as a function of organismal complexity and body size)

      This can all occur even (neah - especially) if there was no positive selection at the organism/population level for the build up of the fore-mentioned bulk DNA.

      Indeed, there wasn't. So what are we arguing over then?

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    26. @ Georgi

      re
      So what are we arguing over then?

      I think I am struggling with


      For something to be an exaptation, it needs to be maintained by purifying selection. Otherwise it's no different from neutral sequences and you can't claim it has a "function"


      Why cannot "functionality" emerge as some later evolutionary after-thought after genome expansion has already occurred? (forgive my clumsy turn of phrase)

      I really need to hit the sack. I will pick up tomorrow.

      Dziękuje ci

      Delete
    27. @ Georgi

      I forgot - if I remember correctly I should have said

      Благодаря ти много! и лека нощ

      and to Claudiu

      Вялікі дзякуй! і спакойнай ночы

      Delete
  14. This comment has been removed by the author.

    ReplyDelete
    Replies
    1. Gary,

      You're a spectacular joke. Don't you get tired of making self-humiliating comments?

      Delete
    2. To help prevent further embarrassing sabotage of my science work I deleted the comment that had a link to a preliminary version of the new software.

      Thanks for reminding me that I was only inviting trouble by mentioning it in a forum like this one.

      Delete
    3. Too late Gary. I copied it and published it under my name in a top tier journal. I told them: this is such a revolutionary idea into such a revolutionary software, that if you don't publish it immediately, someone is going to steal it from me! Obviously, they saw the power of the software and ideas, and published it immediately. They told me that it will break barriers in biology and software engineering, all in one. They were quite impressed.

      Delete
    4. Too late Gary. I copied it and published it under my name in a top tier journal.

      I now feel egged-on.



      Delete
  15. Larry, I hope you have seen the post at UD where Timaeus lectures you about your unworthiness to have firm opinions about evolution. Because you don't regularly publish in the peer-reviewed evolutionary biology literature. Unlike the UD crowd (I assume).

    I mean, it's not like writing a major biochemistry textbook brings with it any requirement to keep up on molecular evolution, right?

    If you can open a thread I suspect commenters here will have a lot of fun with this one.

    ReplyDelete
    Replies
    1. Larry's really gotten under their skin, hasn't he? I notice that post was put up by Barry Arrington, whose extensive publication history in the peer-reviewed scientific literature on evolutionary biology is, of course, well known.

      Delete
    2. They get particularly angry at people whose criticisms are effective. Elizabeth Liddle infuriates them, not because she insults people. She never does that. She is endlessly patient, temperate and clear.

      That is a no-no there if you are not on their side. So she gets denounced as if here style was insulting and dismissive.

      In Larry's case they use his dismissive labeling as an excuse to avoid his arguments.

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    3. I have challenged the host of this blog on UD to provide one piece of evidence out of so "many" that convinced him that LIFE started on it's own.
      I'm not overly demanding I think...


      Delete
    4. I wonder if your opinions on evolutionary biology carry any weight, according to Timaeus's high standards. With just short of 100,000 citations (Google Scholar) and only a moth named after you, it's possible that you would fail to impress Timaeus. Surely if you were a real expert, you could show an Elephas felsensteini for it.

      But evolution is a serious subject, best left to lawyers, philosophers, theologians, preachers, programmers, refrigerator repair men, and whatever Kairosfocus does for a living.

      Delete
    5. @Piotr: show an Elephas felsensteini

      There is one. It's in the room, but no one is talking about it. It has a big P(T|H) on its side.

      Delete
    6. I have many opinions. How valuable are they to you? What would be the determining factor to make my opinions valuable to you?

      Delete
    7. Sorry, KevNick, I was talking to Joe Felsenstein. I don't know what to think of your opinions, since I have never seen them expressed.

      Delete
    8. KevNick, I can’t answer for Dr. Moran, but here is why I think life can form by itself, without the intervention of god(s). Note that we don’t understand the full process at this point! However, we know enough that it seems reasonable to me to expect that someday we may.

      Understanding life’s origin involves looking in two directions, from complex existing live toward the simple molecules from which is may have formed, and from simple molecules toward complex ones found in living systems.

      Looking from living organisms toward their simpler components, we see that the chemistry of living things is wonderful!, amazing!, complex! – but not magic. It is reasonable to expect that the origin of this complex biochemistry is also complex but not magic.

      Looking from simple molecules such as existed on the early earth toward living organisms, several observations show that biochemical complexity can develop naturally. These observations are far from complete, but if these things can happen, it is reasonable to expect that more complex steps can also happen.

      What observations are they? First, simple chemicals present on the early earth can combine to form simple “building block” molecules including various hydrocarbons, amino acids, and nucleotides. These can link to form very short proteins and RNA molecules. RNA and some chemical analogues can catalyze their own replication. RNA molecules capable of self-replication can evolve, change, in the test tube to become better at self-replication. RNA can catalyze production of proteins, even without a cell to work in. Phospholipids can form in the test tube from simple molecules and can form bubbles. When agitated they can concentrate other organic compounds inside the bubbles. People are doing some interesting research into the development of proton (acid) gradients across hydrocarbon layers in porous rock such as found around hydrothermal vents in the ocean, research that may reveal how ATP (used as a “battery” in many cellular processes) can be formed without living things.

      At this point we don’t doing have enough information to know how this all fits together and how living organisms formed. But it is reasonable to think that the limitation is in our understanding, not in what chemicals plus energy can produce naturally.

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    9. bwilson295,

      Nice explanation. However, I would have started by asking how on earth could there be an explanation other than a natural one for the origin of life. Otherwise you're letting that idiot think that it's right to assume that the default position is that god(s)-did-it.

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    10. I have challenged the host of this blog on UD to provide one piece of evidence out of so "many" that convinced him that LIFE started on it's own.

      I know, why can't these durn pointy-headed science types see it's so much less likely that the Universe could evolve a virus or microbe out of some sort of biochemical precursor than that a creator/designer infinitely more powerful, intelligent, and complex than we are popped up out of nowhere?

      Delete
    11. Frankly, I am more amazed that almost all of the Periodic Table is generated by Super Nova thereby validating the lyrics of a Crosby Stills Nash & Young song that we are all "stardust". Talk about simplicity to complexity!

      Abiogenesis seems most unremarkable in comparison!

      Some remarks on this thread are beginning to remind me of one my favorite rock star's aphorisms:


      Some scientists claim that hydrogen, because it is so plentiful, is the basic building block of the universe. I dispute that. I say there is more stupidity than hydrogen, and that is the basic building block of the universe.

      Frank Zappa

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    12. Photosynthesis, you wrote, " I would have started by asking how on earth could there be an explanation other than a natural one for the origin of life. Otherwise you're letting that idiot think that it's right to assume that the default position is that god(s)-did-it." You have a point.

      However, many people, likely including KevNick, have "god(s)-did-it" so deeply intrenched in their brains that suggesting it's not the default position just leads to a failure of communication. So I just briefly summarized evidence, since he asked for that. My reply as intended to suggest to him (and, more importantly, the theoretical other, more open-minded readers) that Dr. Moran's choice not to answer KevNick's question was a decision not to waste time on a red herring, rather than an indication that there is no evidence for natural abiogenesis.

      Delete
    13. Like Joe, I hope Larry will address Timaeus' long, windy ad hominem attack on Larry, which has the neutral title, "Timaeus Exposes Larry Moran."

      http://www.uncommondescent.com/intelligent-design/timaeus-exposes-larry-moran/

      Creationists never "disagree" with scientists, nor "refute" scientists, they only "expose" scientists. (Right-wing propaganda is all about choosing the right verbs for what you do, and then different verbs for what the other guy does. Creationists "share their faith", but evolutionists "impose their religion.")

      The use of the title "Exposes Larry Moran" leads to a sex joke by Mung, UD's greatest wit.

      Timaeus' thesis is that Larry has not published an article on evolutionary theory in > 10 years, therefore any statement Larry makes about evolutionary theory has no authority. This argument is advanced by ID proponents, when NO proponent of Intelligent Design-- not Behe, not Wells, not Dembski, not their founder, lawyer Phillip Johnson-- NO ID proponent has ever published even one article on evolutionary theory. But they know, they just know, that our genome must have no junk, and they just know that junk DNA is a prediction of Darwinism.

      As for Timaeus himself, while he attacks Larry via his publication record, Timaeus won't tell us his publication record, or teaching history, or anything. Timaeus insists on anonymity.

      As usual, the commenters at UD rage against us at Sandwalk because we here call ID proponents "IDiots" when they act like idiots, which is name-calling, and that's bad when we do it. Meanwhile the IDiots take the moral high road, avoiding name-calling and using only devastating ID logic, such as this gem from Axel, who hates scientists with a white-hot fury:

      Yes, nad med. It shouldn’t surprise us that in ridiculing ID and its adherents, such numb-skulls [Psst-- he means us at Sandwalk. -- Diogenes] are ridiculing Einstein’s scientific world-view...

      They are nothing more than ephemeral pimples on the backside of human thought and discovery, as arrogant as they are fatuous.


      Good thing they took the moral high road there. You know, maybe we should stop calling them IDiots even when they act like it. After all, ID proponents don't engage in name-calling.

      You see that, at UD, they're all up there with Einstein. Nothing arrogant about IDers associating themselves with Einstein.

      And here I'd thought that Timaeus, Joe Gallien, Mung, Axel, KairosFocus, and the other UD commenters were all bitter failures at their pathetic non-science careers and wannabe scientists who always falsely inflated their credentials, or flat out lie about them.

      Larry, why can't you be more like ID proponents? And lie about your accomplishments.


      Delete
    14. It's harder to lie when you use your real name. Or at least easier to be, um, exposed when you do.

      Delete
    15. Diogenes,

      Don't be unfair to Michael Behe. Don't be like the UD crowd, and give credit where it's due. He has published a few articles like this one: Behe & Snoke 2004. He may be wrong, but at least Protein Science is a real peer-reviewed journal.

      So they've got Behe and... uh... yeah, they've got Behe. Before Barry banned me, I once pointed out to them that where I work -- a (horribile dictu) humanities faculty at a provincial university in Poland -- people publish more articles in peer-reviewed journals with a larger-than-zero Impact Factor every year than the whole ID movement has produced in its history or will publish before the Sun bloats up into a red giant. So much for their credentials game.

      Delete
    16. Piotr says: Don't be like the UD crowd, and give credit where it's due. He has published a few articles like this one: Behe & Snoke 2004.

      Ya got me there, Piotr, that's one, it's sort-of related to evolutionary theory. It was > 10 years ago, and Behe's had no peer-reviewed articles remotely related to evolutionary theory in > 10 years since-- which is what Timaeus accuses Larry of.

      And Behe and Snoke 2004 has been so well-received in the literature since! Having been mentioned fairly often... by authors citing Behe and Snoke to refute their premises, methods and conclusions.

      Michael Lynch (2005). "Simple evolutionary pathways to complex proteins". Protein Science 14 (9): 2217–2225. doi:10.1110/ps.041171805. PMC 2253472. PMID 16131652

      A big stomp-down on Behe and Snoke. But hey, what would Michael Lynch know about evolutionary genomics?

      And

      Bridgham JT, Carroll SM, Thornton JW. Evolution of hormone-receptor complexity by molecular exploitation. Science 2006 Apr 7;312(5770):97-101.

      specifically cites Behe and Snoke to refute them. But what would Thornton, Sean Carroll or Bridgham know about evolution of binding sites?

      Durrett and Schmidt 2008 (pdf) mentions Behe and Snoke by name while refuting their math.

      and

      Masel, Joanna (March 2006). "Cryptic Genetic Variation Is Enriched for Potential Adaptations". Genetics 172 (3): 1985–1991. doi:10.1534/genetics.105.051649. PMC 1456269. PMID 16387877

      and

      Afriat, Livnat; Cintia Roodveldt; Giuseppe Manco; Dan S. Tawfik (November 21, 2006). "The Latent Promiscuity of Newly Identified Microbial Lactonases Is Linked to a Recently Diverged Phosphotriesterase" (PDF). Biochemistry 45 (46). doi:10.1021/bi061268r

      etc. Yeah, Behe and Snoke got noticed, all right.

      Delete
    17. Piotr: "Before Barry banned me"

      Ah, the defenders of freedom, critical thinking and debate got another debater! Join the very large club.

      Delete
  16. For some reason I always thought that evidence is the most effective tool in criticism of science. I guess, due to the lack of such tools, many pseudo scientists had to develop a new method of defending their predetermined beliefs. Times must've changed ever since the true science ran out of evidence and ideas.

    ReplyDelete
    Replies
    1. You mean like your evidence that life started because some imaginary being created it? Like that?

      Delete
    2. KevNick says "true science ran out of evidence and ideas." What crap!

      Is that a scientific statement? Yes or no. If no, what is it, an emotional outburst, propaganda, etc.? Why should we care then. If yes, it's a scientific statement, why should we trust it? It can't be backed up by evidence, because you just said science ran out of evidence. So you make statements you cannot back up with evidence.

      Since you think science sucks, let's compare it to pseudoscience. What new evidence or ideas has pseudoscience produced in 50 years? Henry Morris wrote "The Genesis Flood" 54 years ago. Creationism since then has had no new ideas in all that time. No YEC has gotten even one inch closer to explaining how light from distant stars got here in 6,000 years, or why radiometric dating shows rocks are old, or why so many diverse kinds of marsupials live in Australia, or why human and dinosaur fossils are never found together, etc. No new ideas in 54 years.

      What new ideas has intelligent design presented? Michael Behe wrote "Darwin's Black Box" 19 years ago and it was shown > 10 years ago that all the systems he called "irreducibly complex" exist in reduced forms somewhere, and/or have evolutionary pathways that are pretty obvious and lead to testable, confirmed predictions. Like the evolution of the immune system and the blood clotting cascade.

      But even in 1996, Behe's idea of "irreducible complexity" was very old. Hitler's mentor, the fanatical anti-Dsrwinist Houston Stewart Chamberlain used that idea under a different name and applied it to the bacterial flagellum, the icon of Intelligent Design, in his 1905 book "Immanuel Kant", chapter 6. Centuries before that, the notion that all parts must be present simultaneously in order for a system to function was used by preformationists to "prove" that an embryo must grow from a tiny homunculus in the father's sperm cell, because any half-formed, intermediate step would kill the organism, so no *natural* process could make an embyo. Such old ideas.

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    3. Thanks KevNick. Now back to church with you, and for the sake of your own dignity and sanity, stop pretending you care about, or know anything of, the human pursuit of scientific knowledge. Maybe god has different plans for you.

      Delete
    4. "Centuries before that, the notion that all parts must be present simultaneously in order for a system to function was used by preformationists to "prove" that an embryo must grow from a tiny homunculus in the father's sperm cell, because any half-formed, intermediate step would kill the organism, so no *natural* process could make an embyo. Such old ideas."

      That is very very interesting Diogenes. Thanks.

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    5. This fellow, Nicholas Malebranche, went even further. He believed that each tiny homunculus had a tinier one inside; and the tinier one contained an even tinier one, and so an infinitum.

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    6. Kevnick,

      You have an invitation to the "church of sanity" from the real scientists. They have not only all the answers but more so, the evidence.

      They have the evidence on how lifeless matter became alive by accident without the need of intelligence. They can't replicate it with all the scientific knowledge and technology they have (where does leave their intelligence in comparison to unintelligent accident?) and yet they call people who demand evidence for their "scientific beliefs" stupid idiots, uneducated morons and blind believers in gods.

      Don't miss a chance! The "church of sanity"-atheism based on "scientific evidence"- is just around the corner.

      Don't miss their favorite first commandment: "scientists don't know, so gods did it". Let them provide you with the third option.

      Have a good laugh!

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    7. Photosynthesis, I cannot take credit for the analogy between ID irreducible complexity and preformationism. It's from Tom Scharle.

      http://www.talkreason.org/articles/chickegg.cfm

      I steal from the best.

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